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Alarmin cytokines including IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) function as danger signals to trigger host immunity in response to tissue injury caused by pathogenic factors such as parasitic infections. Parasitic diseases also provide an excellent context to study their functions and mechanisms. Numerous studies have indicated that alarmin cytokine released by non-immune cells such as epithelial and stromal cells induce the hosts to initiate a type 2 immunity that drives parasite expulsion but also host pathology such as tissue injury and fibrosis. By contrast, alarmin cytokines especially IL-33 derived from immune cells such as dendritic cells may elicit an immuno-suppressive milieu that promotes host tolerance to parasites. Additionally, the role of alarmin cytokines in parasite infections is reported to depend on species of parasites, cellular source of alarmin cytokines, and immune microenvironment, all of which is relevant to the parasitic sites or organs. This narrative review aims to provide information on the crucial and diverse role of alarmin cytokines in parasitic infections involved in different organs including intestine, lung, liver and brain., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Xing, Liu and He.)

The effect of sex on the prevalence and severity of parasitic diseases is an emerging area of research. Several factors underlie sex-based differences, including sociocultural influences that affect exposure to parasites, and physiological disparities linked to biological sex. Hence, human studies must be interpreted cautiously; however, studies conducted under controlled laboratory conditions are important to validate findings in humans. Such research can more effectively elucidate the role of sex-determining physiological factors (particularly their impact on immune responses), as well as the role of sex-specific differences in resistance to, or severity of, parasitic diseases. This review focuses on the overarching impact of biological sex variables on immunity. Both human and rodent experimental data are discussed, with a focus on selected protozoan and helminth infections., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Parasitic diseases have a significant impact on human and animal health, representing a major hazard to the public and causing economic and health damage worldwide. Extracellular vesicles (EVs) have long been recognized as diagnostic and therapeutic tools but are now also known to be implicated in the natural history of parasitic diseases and host immune response modulation. Studies have shown that EVs play a role in parasitic disease development by interacting with parasites and communicating with other types of cells. This review highlights the most recent research on EVs and their role in several aspects of parasite-host interactions in five key parasitic diseases: Chagas disease, malaria, toxoplasmosis, leishmaniasis and helminthiases. We also discuss the potential use of EVs as diagnostic tools or treatment options for these infectious diseases., (© 2024 The Author(s). Journal of Extracellular Vesicles published by Wiley Periodicals LLC on behalf of International Society for Extracellular Vesicles.)

Introduction: The emergence of antiparasitic drug resistance poses a concerning threat to animals and humans. Mesenchymal Stem Cells (MSCs) have been widely used to treat infections in humans, pets, and livestock. Although this is an emerging field of study, the current review outlines possible mechanisms and examines potential synergism in combination therapies and the possible harmful effects of such an approach., Areas Covered: The present study delved into the latest pre-clinical research on utilizing MSCs to treat parasitic infections. As per investigations, the introduction of MSCs to patients grappling with parasitic diseases like schistosomiasis, malaria, cystic echinococcosis, toxoplasmosis, leishmaniasis, and trypanosomiasis has shown a reduction in parasite prevalence. This intervention also alters the levels of both pro- and anti-inflammatory cytokines. Furthermore, the combined administration of MSCs and antiparasitic drugs has demonstrated enhanced efficacy in combating parasites and modulating the immune response., Expert Opinion: Mesenchymal stem cells are a potential solution for addressing parasitic drug resistance. This is mainly because of their remarkable immunomodulatory abilities, which can potentially help combat parasites' resistance to drugs.

Parasitic diseases are a serious global health concern, causing many common and severe infections, including Chagas disease, leishmaniasis, and schistosomiasis. The NLRP3 inflammasome belongs to the NLR (nucleotide-binding domain leucine-rich-repeat-containing proteins) family, which are cytosolic proteins playing key roles in the detection of pathogens. NLRP3 inflammasomes are activated in immune responses to Plasmodium, Leishmania, Toxoplasma gondii, Entamoeba histolytica, Trypanosoma cruzi, and other parasites. The role of NLRP3 is not fully understood, but it is a crucial component of the innate immune response to parasitic infections and its functions as a sensor triggering the inflammatory response to the invasive parasites. However, while this response can limit the parasites' growth, it can also result in potentially catastrophic host pathology. This makes it essential to understand how NLRP3 interacts with parasites to initiate the inflammatory response. Plasmodium hemozoin, Leishmania glycoconjugate lipophosphoglycan (LPG) and E. histolytica Gal/GalNAc lectin can stimulate NLRP3 activation, while the dense granule protein 9 (GRA9) of T. gondii has been shown to suppress it. Several other parasitic products also have diverse effects on NLRP3 activation. Understanding the mechanism of NLRP3 interaction with these products will help to develop advanced therapeutic approaches to treat parasitic diseases. This review summarizes current knowledge of the NLRP3 inflammasome's action on the immune response to parasitic infections and aims to determine the mechanisms through which parasitic molecules either activate or inhibit its action., (© 2024 The Author(s).)

Introduction: Protein microarray is a promising immunomic approach for identifying biomarkers. Based on our previous study that reviewed parasite antigens and recent parasitic omics research, this article expands to include information on vector-borne parasitic diseases (VBPDs), namely, malaria, schistosomiasis, leishmaniasis, babesiosis, trypanosomiasis, lymphatic filariasis, and onchocerciasis., Areas Covered: We revisit and systematically summarize antigen markers of vector-borne parasites identified by the immunomic approach and discuss the latest advances in identifying antigens for the rational development of diagnostics and vaccines. The applications and challenges of this approach for VBPD control are also discussed., Expert Opinion: The immunomic approach has enabled the identification and/or validation of antigen markers for vaccine development, diagnosis, disease surveillance, and treatment. However, this approach presents several challenges, including limited sample size, variability in antigen expression, false-positive results, complexity of omics data, validation and reproducibility, and heterogeneity of diseases. In addition, antigen involvement in host immune evasion and antigen sensitivity/specificity are major issues in its application. Despite these limitations, this approach remains promising for controlling VBPD. Advances in technology and data analysis methods should continue to improve candidate antigen identification, as well as the use of a multiantigen approach in diagnostic and vaccine development for VBPD control.

Infections caused by parasites and fungi can trigger the cytokine storm syndrome (CSS). These infections causing CSS can occur together with acquired immunodeficiencies, lymphomas, the use of immunosuppressive medications, transplant recipients, cancer, autoinflammatory, and autoimmune diseases or less frequently in healthy individuals. Histoplasma, Leishmania, Plasmodium, and Toxoplasma are the most frequent organisms associated with a CSS. It is very important to determine a previous travel history when evaluating a patient with a CSS triggered by these organisms as this may be the clue to the causal agent. Even though CSS is treated with specific therapies, an effort to find the causal organism should be carried out since the treatment of the infectious organism may stop the CSS. Diagnosing a CSS in the presence of parasitic or fungal sepsis should also lead to the study of an altered cytotoxic or hemophagocytic response in the susceptible host., (© 2024. The Author(s), under exclusive license to Springer Nature Switzerland AG.)

Neglected tropical parasitic diseases (NTD) are prevalent in many countries and cost-effective treatments remain urgently needed. Novel approaches have been proposed to address these diseases through an action on immune co-inhibitory checkpoints which are exploited by parasites to evade the immune system. Among these checkpoints, TIM-3 has been shown to play a key role in antiparasitic immunity via a repression and functional attenuation of CD4 + and/or CD8 + T-cells. The present review discusses the role of the TIM-3/galectin-9 checkpoint in seven major NTD: Chagas disease, leishmaniasis and malaria (3 trypanosomatid infections), schistosomiasis, toxoplasmosis, echinococcosis and filariasis (4 helminth infections). In each case, the role of the checkpoint has been analyzed and the use of anti-TIM-3 antibodies evaluated as a potential therapeutic approach. In general, the parasitic infection is coupled with an upregulation of TIM-3 expressed on T cells, but not necessarily with an exhaustion of those T cells. In several cases, the use of anti-TIM-3 antibodies represent a possible strategy to reinforce the clearance and to reduce the parasite load. Promising data have been reported in cases of leishmaniasis, malaria and schistosomiasis, whereas a similar approach proved much less efficient (if not deleterious) in cases of echinococcosis and the Chagas disease. Nevertheless, the TIM-3 checkpoint warrants further consideration as a potential immune target to combat these pathologies, using antibodies or drugs capable of reducing directly or indirectly the expression and function of the checkpoint, to restore an immune control., Competing Interests: Conflict of interest The author declares no conflict of interest., (Copyright © 2022. Published by Elsevier B.V.)

The adaptive immune system is critical to an effective response to infection in vertebrates, with T-helper (Th) cells pivotal in orchestrating these responses. In natural populations where co-infections are the norm, different Th responses are likely to play an important role in maintaining host health and fitness, a relationship which remains poorly understood in wild animals. In this study, we characterised variation in functionally distinct Th responses in a wild population of Soay sheep by enumerating cells expressing Th-subset specific transcription factors and quantifying Th-associated cytokines. We tested the prediction that raised Th1 and Th2 responses should predict reduced apicomplexan and helminth parasite burdens, respectively. All measures of Th-associated cytokine production increased with age, while Th17- and regulatory Th-associated cytokine production increased more rapidly with age in males than females. Independent of age, sex, and each other, IL-4 and Gata3 negatively predicted gastro-intestinal nematode faecal egg count, while IFN-γ negatively predicted coccidian faecal oocyst count. Our results provide important support from outside the laboratory that Th1 and Th2 responses predict resistance to different kinds of parasites, and illustrate how harnessing specific reagents and tools from laboratory immunology will illuminate our understanding of host-parasite interactions in the wild., (© 2022. The Author(s).)

Human Leukocyte Antigen-G (HLA-G), a polymorphic non-classical HLA (HLA-Ib) with immune-regulatory properties in cancers and infectious diseases, presents both membrane-bound and soluble (sHLA-G) isoforms. Polymorphism has implications in host responses to pathogen infections and in pathogenesis. Differential expression patterns of HLA-G/sHLA-G or its polymorphism seem to be related to different pathological conditions, potentially acting as a disease progression biomarker. Pathogen antigens might be involved in the regulation of both membrane-bound and sHLA-G levels and impact immune responses during co-infections. The upregulation of HLA-G in viral and bacterial infections induce tolerance to infection. Recently, sHLA-G was found useful to identify the prognosis of Coronavirus disease 2019 (COVID-19) among patients and it was observed that the high levels of sHLA-G are associated with worse prognosis. The use of pathogens, such as Plasmodium falciparum , as immune modulators for other infections could be extended for the modulation of membrane-bound HLA-G in COVID-19-infected tissues. Overall, such information might open new avenues concerning the effect of some pathogens such as parasites in decreasing the expression level of HLA-G to restrict pathogenesis in some infections or to influence the immune responses after vaccination among others.

Maternal infection during pregnancy is known to alter the development and function of offspring's immune system, leading to inappropriate immune responses to common childhood infections and immunizations. Although this is an expanding field, maternal parasitic infections remain understudied. Millions of women of reproductive age are currently at risk for parasitic infection, whereas many pregnant, chronically infected women are excluded from mass drug administration due partially to a lack of resources, as well as fear of unknown adverse fetal developmental outcomes. In areas endemic for multiple parasitic infections, such as sub-Saharan Africa, there are increased rates of morbidity and mortality for various infections during early childhood in comparison with nonendemic areas. Despite evidence supporting similar immunomodulatory effects between various parasite species, there is no clear mechanistic understanding of how maternal infection reprograms offspring immunity. This brief review will compare the effects of selected maternal parasitic infections on offspring immunity., (Copyright © 2022 by The American Association of Immunologists, Inc.)

Hosts diverge widely in how, and how well, they defend themselves against infection and immunopathology. Why are hosts so heterogeneous? Both epidemiology and life history are commonly hypothesized to influence host immune strategy, but the relationship between immune strategy and each factor has commonly been investigated in isolation. Here, we show that interactions between life history and epidemiology are crucial for determining optimal immune specificity and sensitivity. We propose a demographically-structured population dynamics model, in which we explore sensitivity and specificity of immune responses when epidemiological risks vary with age. We find that variation in life history traits associated with both reproduction and longevity alters optimal immune strategies-but the magnitude and sometimes even direction of these effects depends on how epidemiological risks vary across life. An especially compelling example that explains previously-puzzling empirical observations is that depending on whether infection risk declines or rises at reproductive maturity, later reproductive maturity can select for either greater or lower immune specificity, potentially illustrating why studies of lifespan and immune variation across taxa have been inconclusive. Thus, the sign of selection on the life history-immune specificity relationship can be reversed in different epidemiological contexts. Drawing on published life history data from a variety of chordate taxa, we generate testable predictions for this facet of the optimal immune strategy. Our results shed light on the causes of the heterogeneity found in immune defenses both within and among species and the ultimate variability of the relationship between life history and immune specificity., Competing Interests: The authors have declared that no competing interests exist.

The human host immune responses to parasitic infections are complex. They can be categorized into four immunological pathways mounted against four types of parasitic infections. For intracellular protozoa, the eradicable host immunological pathway is TH1 immunity involving macrophages (M1), interferon gamma (IFNγ) CD4 T cells, innate lymphoid cells 1 (NKp44+ ILC1), CD8 T cells (Effector-Memory4, EM4), invariant natural killer T cells 1 (iNKT1) cells, and immunoglobulin G3 (IgG3) B cells. For intracellular protozoa, the tolerable host immunological pathway is TH1-like immunity involving macrophages (M2), interferon gamma (IFNγ)/TGFβ CD4 T cells, innate lymphoid cells 1 (NKp44- ILC1), CD8 T cells (EM3), invariant natural killer T 1 (iNKT1) cells, and immunoglobulin A1 (IgA1) B cells. For free-living extracellular protozoa, the eradicable host immunological pathway is TH22 immunity involving neutrophils (N1), interleukin-22 CD4 T cells, innate lymphoid cells 3 (NCR+ ILC3), iNKT17 cells, and IgG2 B cells. For free-living extracellular protozoa, the tolerable host immunological pathway is TH17 immunity involving neutrophils (N2), interleukin-17 CD4 T cells, innate lymphoid cells 3 (NCR- ILC3), iNKT17 cells, and IgA2 B cells. For endoparasites (helminths), the eradicable host immunological pathway is TH2a immunity with inflammatory eosinophils (iEOS), interleukin-5/interleukin-4 CD4 T cells, interleukin-25 induced inflammatory innate lymphoid cells 2 (iILC2), tryptase-positive mast cells (MCt), iNKT2 cells, and IgG4 B cells. For ectoparasites (parasitic insects and arachnids), the eradicable host immunological pathway is TH2b immunity with inflammatory basophils, chymase- and tryptase-positive mast cells (MCct), interleukin-3/interleukin-4 CD4 T cells, interleukin-33 induced nature innate lymphoid cells 2 (nILC2), iNKT2 cells, and immunoglobulin E (IgE) B cells. The tolerable host immunity against ectoparasites and endoparasites is TH9 immunity with regulatory eosinophils, regulatory basophils, interleukin-9 mast cells (MMC9), thymic stromal lymphopoietin induced innate lymphoid cells 2, interleukin-9 CD4 T cells, iNKT2 cells, and IgA2 B cells. In addition, specific transcription factors important for specific immune responses were listed. This JAK/STAT signaling is key to controlling or inducing different immunological pathways. In sum, Tfh is related to STAT5β, and BCL6 expression. Treg is related to STAT5α, STAT5β, and FOXP3. TH1 immunity is related to STAT1α, STAT4, and T-bet. TH2a immunity is related to STAT6, STAT1α, GATA1, and GATA3. TH2b immunity is related to STAT6, STAT3, GATA2, and GATA3. TH22 immunity is associated with both STAT3α and AHR. THαβ immunity is related to STAT1α, STAT1β, STAT2, STAT3β, and ISGF. TH1-like immunity is related to STAT1α, STAT4, STAT5α, and STAT5β. TH9 immunity is related to STAT6, STAT5α, STAT5β, and PU.1. TH17 immunity is related to STAT3α, STAT5α, STAT5β, and RORG. TH3 immunity is related to STAT1α, STAT1β, STAT2, STAT3β, STAT5α, STAT5β, and ISGF. This categorization provides a complete framework of immunological pathways against four types of parasitic infections. This framework as well as relevant JAK/STAT signaling can provide useful knowledge to control allergic hypersensitivities and parasitic infections via development of vaccines or drugs in the near future.

Cell death is an essential immunological apparatus of host defense, but dysregulation of mutually inclusive cell deaths poses severe threats during microbial and parasitic infections leading to deleterious consequences in the pathological progression of infectious diseases. Nucleotide-binding oligomerization domain (NOD)-Leucine-rich repeats (LRR)-containing receptors (NLRs), also called nucleotide-binding oligomerization (NOD)-like receptors (NLRs), are major cytosolic pattern recognition receptors (PRRs), their involvement in the orchestration of innate immunity and host defense against bacteria, viruses, fungi and parasites, often results in the cleavage of gasdermin and the release of IL-1β and IL-18, should be tightly regulated. NLRs are functionally diverse and tissue-specific PRRs expressed by both immune and non-immune cells. Beyond the inflammasome activation, NLRs are also involved in NF-κB and MAPK activation signaling, the regulation of type I IFN (IFN-I) production and the inflammatory cell death during microbial infections. Recent advancements of NLRs biology revealed its possible interplay with pyroptotic cell death and inflammatory mediators, such as caspase 1, caspase 11, IFN-I and GSDMD. This review provides the most updated information that caspase 8 skews the NLRP3 inflammasome activation in PANoptosis during pathogen infection. We also update multidimensional roles of NLRP12 in regulating innate immunity in a content-dependent manner: novel interference of NLRP12 on TLRs and NOD derived-signaling cascade, and the recently unveiled regulatory property of NLRP12 in production of type I IFN. Future prospects of exploring NLRs in controlling cell death during parasitic and microbial infection were highlighted.

Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Antiviral, antibacterial, and antiparasitic drugs and vaccines are essential to maintaining the health of humans and animals. Yet, their production can be slow and expensive, and efficacy lost once pathogens mount resistance. Chicken immunoglobulin Y (IgY) is a highly conserved homolog of human immunoglobulin G (IgG) that has shown benefits and a favorable safety profile, primarily in animal models of human infectious diseases. IgY is fast-acting, easy to produce, and low cost. IgY antibodies can readily be generated in large quantities with minimal environmental harm or infrastructure investment by using egg-laying hens. We summarize a variety of IgY uses, focusing on their potential for the detection, prevention, and treatment of human and animal infections., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Lee, Samardzic, Wallach, Frumkin and Mochly-Rosen.)

The role of p53 in tumor suppression has been extensively studied and well-established. However, the role of p53 in parasitic infections and the intestinal type 2 immunity is unclear. Here, we report that p53 is crucial for intestinal type 2 immunity in response to the infection of parasites, such as Tritrichomonas muris and Nippostrongylus brasiliensis. Mechanistically, p53 plays a critical role in the activation of the tuft cell-IL-25-type 2 innate lymphoid cell circuit, partly via transcriptional regulation of Lrmp in tuft cells. Lrmp modulates Ca 2+ influx and IL-25 release, which are critical triggers of type 2 innate lymphoid cell response. Our results thus reveal a previously unrecognized function of p53 in regulating intestinal type 2 immunity to protect against parasitic infections, highlighting the role of p53 as a guardian of immune integrity.

As a relatively successful pathogen, several parasites can establish long-term infection in host. This "harmonious symbiosis" status relies on the "precise" manipulation of host immunity and metabolism, however, the underlying mechanism is still largely elusive. Immunometabolism is an emerging crossed subject in recent years. It mainly discusses the regulatory mechanism of metabolic changes on reprogramming the key transcriptional and post-transcriptional events related to immune cell activation and effect, which provides a novel insight for understanding how parasites regulate the infection and immunity in hosts. The present study reviewed the current research progress on metabolic reprogramming mechanism exploited by parasites to modulate the function in various immune cells, highlighting the future exploitation of key metabolites or metabolic events to clarify the underlying mechanism of anti-parasite immunity and design novel intervention strategies against parasitic infection., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Chen, Zhou and Pan.)

Knowledge of glycogen synthase kinase 3β (GSK3β) activity and the molecules identified that regulate its function in infections caused by pathogenic microorganisms is crucial to understanding how the intensity of the inflammatory response can be controlled in the course of infections. In recent years many reports have described small molecular weight synthetic and natural compounds, proteins, and interference RNA with the potential to regulate the GSK3β activity and reduce the deleterious effects of the inflammatory response. Our goal in this review is to summarize the most recent advances on the role of GSK3β in the inflammatory response caused by bacteria, bacterial virulence factors (i.e. LPS and others), viruses, and parasites and how the regulation of its activity, mainly its inhibition by different type of molecules, modulates the inflammation., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Cortés-Vieyra, Silva-García, Gómez-García, Gutiérrez-Castellanos, Álvarez-Aguilar and Baizabal-Aguirre.)

Parasitic plants pose a major biotic threat to plant growth and development and lead to losses in crop productivity of billions of USD annually. By comparison with "normal" autotrophic plants, parasitic plants live a heterotrophic lifestyle and rely on water, solutes and to a greater (holoparasitic plants) or lesser extent (hemiparasitic plants) on sugars from other host plants. Most hosts are unable to detect an infestation by plant parasites or unable to fend off these parasitic invaders. However, a few hosts have evolved defense strategies to avoid infestation or protect themselves actively post-attack often leading to full or partial resistance. Here, we review the current state of our understanding of the defense strategies to plant parasitism used by host plants with emphasis on the active molecular resistance mechanisms. Furthermore, we outline the perspectives and the potential of future studies that will be indispensable to develop and breed resistant crops., (© American Society of Plant Biologists 2020. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

B lymphocytes are primarily well known for their contribution to immunity by antibody production, antigen presentation and, the production of cytokines. In recent years several studies demonstrated the existence of B cells with regulatory functions, which have been termed regulatory B cells (B regs ), similar to regulatory T cells (T regs ). B regs are a subpopulation of B cells that have immunosuppressive effects via the production of regulatory cytokines including interleukin-10 (IL-10), transforming growth factor-β (TGF-β), and IL-35. B regs limit host defense against various pathogens. In addition, B regs contribute to increased levels of regulatory cytokines and leads to an induction of suppressive T regs , which exert broader suppressive functions against various pathogens. The high percentage of B regs is positively associated with viral and bacterial load and can contribute to poor vaccine responses. B regs can also facilitate pathogen survival at an early stage of infection, and subsequently cause increased severity of disease by inhibiting pro-inflammatory cytokine production, macrophage activation, and inflammatory T cells activation such as Th1, Th17, and Th22. Also, B regs afford protection against the hyper-inflammatory response in parasitic infections. Here we review the central role of B regs in many major bacterial and viral human infections, and provide an overview of the immunoregulatory mechanisms used by B regs ., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Parasitic organisms of various genera have threatened humankind. Although they are not always fatal but can damage the well-being of an individual in terms of both economic and societal crisis. Marked progress has been made toward eliminating those pathogenic organisms, however, complete removal is still not possible. Several antiparasitic drug moieties have been largely commercialized and are routinely used at the same time novel drug candidates are still required. Programmed cell death (PCD) is a vital biological phenomenon inside every organism. Particularly, induction of the death signaling inside the parasitic species through selective targeting of effective drug candidates is one of the major strategies to combat these infectious organisms. In this chapter significance of apoptosis induction to eliminate the parasitic disease has been illustrated with suitable references. Moreover, we have shared our own experiences of apoptosis induction in eliminating a World Health Organization enlisted Neglected Tropical Disease, lymphatic filariasis. On the other hand, we have also tried to put some light on the mechanism of apoptosis in different parasites., Competing Interests: Conflict of interest None., (Copyright © 2021 Elsevier Inc. All rights reserved.)

For decades, glucocorticoids (GC) have been used to treat several inflammatory conditions, including chronic and autoimmune diseases, due to their potent anti-inflammatory properties. In the context of infectious diseases, the use of GCs may be effective as adjuvant to antibiotic therapy by controlling excessive inflammatory responses resulting in better outcome in some cases. However, the use of GCs has been associated with a vast number of side effects, including increased probability of immunosuppression and consequent risk of opportunistic infection. Glucocorticoid-induced leucine zipper (GILZ) and Annexin A1 (AnxA1) are GC-induced proteins intrinsically involved with the anti-inflammatory functions of GCs without the associated adverse metabolic effects. Recent studies have shown that these GC-proteins exhibit pro-resolving effects. An essential characteristic of pro-resolving molecules is their ability to coordinate the resolution of inflammation and promote host defense in most experimental models of infection. Although the role of GILZ and AnxA1 in the context of infectious diseases remain to be better explored, herein we provide an overview of the emerging functions of these GC-proteins obtained from pre-clinical models of infectious diseases., (Copyright © 2020 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

The circadian clock provides organisms with the ability to track time of day, allowing them to predict and respond to cyclical changes in the external environment. In mammals this clock consists of multiple auto-regulatory feedback loops generated by a network of circadian clock proteins. This network provides the fundamental basis for rhythms in behaviour and physiology. This clockwork machinery exists in most cells, including those of the immune system. In recent years evidence has emerged highlighting the important role of molecular clocks in dictating the response of immune pathways. While initial work highlighted the effect of the clock in the 'first line of defence', the innate immune system, it has become increasingly apparent that it also plays a role in the more tailored, later-stage adaptive immune response. This review provides an overview of the role of the circadian cycle in the adaptive immune response. We interrogate the depth of knowledge on cell intrinsic clocks within adaptive immune cells and how these cells may be temporally directed by extrinsic rhythmic signals. We discuss the role of the circadian clock in diseases associated with adaptive immunity such as multiple sclerosis, asthma and parasitic infection. We also discuss the current knowledge on timing of vaccination, and the implications this may have on how we can harness and modulate temporal gating of the adaptive immune response in a clinical setting., (© 2019 John Wiley & Sons Ltd.)

Humans and crown catarrhines evolved with the inability to synthesize the oligosaccharide galactose-α-1,3-galactose (α-Gal). In turn, they naturally produce high quantities of the glycan-specific antibodies that can be protective against infectious agents exhibiting the same carbohydrate modification on their surface coat. The protective immunity induced by α-Gal is ensured through an antibody-mediated adaptive and cell-mediated innate immune response. Therefore, the α-Gal antigen represents an attractive and feasible target for developing glycan-based vaccines against multiple diseases. In this review article we provide an insight into our current understanding of the mechanisms involved in the protective immunity to α-Gal and discuss the possibilities and challenges in developing a single-antigen pan-vaccine for prevention and control of parasitic diseases of medical and veterinary concern., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Russian wheat aphid, Diuraphis noxia (Kurdjumov), is a severe pest of wheat, Triticum aestivum L., throughout the world. Resistant cultivars are viewed as the most economical and environmentally viable control available. Studies to identify molecular markers to facilitate resistance breeding started in the 1990s, and still continue. This paper reviews and discusses the literature pertaining to the D. noxia R-genes on chromosome 7D, and markers reported to be associated with them. Individual plants with known phenotypes from a panel of South African wheat accessions are used as examples. Despite significant inputs from various research groups over many years, diagnostic markers for resistance to D. noxia remain elusive. Factors that may have impeded critical investigation, thus blurring the accumulation of a coherent body of information applicable to Dn resistance, are discussed. This review calls for a more fastidious approach to the interpretation of results, especially considering the growing evidence pointing to the complex regulation of aphid resistance response pathways in plants. Appropriate reflection on prior studies, together with emerging knowledge regarding the complexity and specificity of the D. noxia -wheat resistance interaction, should enable scientists to address the challenges of protecting wheat against this pest in future.

Background: Altered hypothalamic-pituitary-adrenal (HPA) function and related changes in circulating glucocorticoids have been implicated in the pathogenesis of numerous diseases that involve dysregulated immune function. Glucocorticoid hormones have both direct and indirect modulatory effects on both pro- and anti-inflammatory aspects of the immune system, including granulocytic and lymphocytic leukocyte subsets. However, past findings are complicated by inconsistencies across studies in how glucocorticoids and immune markers interact and relate to disease risk. Some incongruencies are likely due to an overreliance on single-unit (e.g., HPA or one immune marker) measures, and a failure to consider ecological exposures that may shape the base levels or correspondence between these systems. Here, we test single-unit and diurnal measures of HPA axis and immune system interactions in a less-industrial ecological setting with relatively high parasite loads., Methods: In a sample of 114 Honduran women (mean age = 36 years), morning and evening blood samples were analyzed to quantify granulocytes, lymphocytes, and immunoglobulin-E (IgE). Saliva was collected over 2 days (8 samples per woman) to measure peak cortisol, cumulative cortisol, and slope of decline. These repeated measures of saliva and venous blood were used to investigate associations between single-point and diurnal salivary cortisol and leukocytes, under variable levels of past parasite exposure (proxied by IgE)., Results: Individuals with less of a decline in cortisol (i.e., "flatter" decline) show less of an increase in lymphocytes (2.27% increase in cells/μL/hr; 95% CI: 0.91-7.29; p = .01) across the day compared to those with steeper cortisol decline (7.5% increase in lymphocytes; 95% CI: 5.79-9.34; p < .001). IgE levels did not modify this association. Interestingly, IgE did moderate relationships between measures of cortisol and granulocytes: diurnal cortisol was positively associated with granulocytes, only in individuals with high previous exposure to parasites. There were no consistent relationships between single-unit measures of cortisol, lymphocytes or granulocytes, regardless of past parasite exposure., Discussion: Results demonstrate that the relationship between HPA function and immune modulation cannot be fully understood without an understanding of local disease ecology. These results highlight the importance of research that seeks to identify etiologies of disease across environmental contexts., (© 2020 Wiley Periodicals LLC.)

Parasites, bacteria, and viruses pose serious threats to public health. Many parasite infections, including infections of protozoa and helminths, can inhibit inflammatory responses and impact disease outcomes caused by viral, bacterial, or other parasitic infections. Type I interferon (IFN-I) has been recognized as an essential immune effector in the host defense against various pathogens. In addition, IFN-I responses induced by co-infections with different pathogens may vary according to the host genetic background, immune status, and pathogen burden. However, there is only limited information on the roles of IFN-I in co-infections with parasites and viruses, bacteria, or other parasites. This review summarizes some recent findings on the roles of IFN-I in co-infections with parasites, including Leishmania spp., Plasmodium spp., Eimeria maxima, Heligmosomoides polygyrus, Brugia malayi , or Schistosoma mansoni , and viruses or bacteria and co-infections with different parasites (such as co-infection with Neospora caninum and Toxoplasma gondii , and co-infection with Plasmodium spp. and H. polygyrus ). The potential mechanisms of host responses associated with co-infections, which may provide targets for immune intervention and therapies of the co-infections, are also discussed., (Copyright © 2020 Ma, Su and Lu.)

Neutrophil extracellular trap (NET) is a type of bead-like, fibrous and reticular substances that is actively released by activated inflammatory neutrophils during the stage of infections or inflammatory responses. NET, which is composed of chromatin DNA and multiple intracellular protein components, may wrap pathogens to limit their diffusions. Meanwhile, NET may kill pathogens via a wide range of antibacterial proteins, which is considered as the third antibacterial mechanism of neutrophils, in addition to phagocytosis and degranulation. Recent studies have shown the involvement of NET in the immune response against parasitic infections. This review summarizes the advances of NETs in the immune responses against parasitic infections, so as to provide insights into the elucidation of the pathogenesis and development of therapeutics of parasitic diseases.

Kudoa septempunctata is a myxozoan parasite that causes food poisoning in individuals consuming olive flounder. The present study aimed to investigate the currently insufficiently elucidated early molecular mechanisms of inflammatory responses in the intestine owing to parasite ingestion. After Kudoa spores were isolated from olive flounder, HT29 cells were exposed to spores identified to be alive using SYTO-9 and propidium iodide staining or to antigens of Kudoa spores (KsAg). IL-1β, IL-8, TNF-α and NFKB1 expression and NF-κB activation were assessed using real-time PCR, cytokine array and western blotting. The immunofluorescence of FITC-conjugated lectins, results of ligand binding assays using Mincle-Fc and IgG-Fc, CLEC4E expressions in response to KsAg stimulation, and Mincle-dependent NF-κB activation were assessed to clarify the early immunetriggering mechanism. Inflammatory cytokines (IL-1α, GM-CSF and TNF-α), chemokines (IL-8, CCL2, CCL5 and CXCL1) and NF-κB activation (pNF-κB/NF-κB) in HT29 cells increased following stimulation by KsAg. The immunofluorescence results of spores and lectins (concanavalin A and wheat germ agglutinin) suggested the importance of Mincle in molecular recognition between Kudoa spores and intestinal cells. Practically, data for Mincle-Fc and KsAg binding affinity, CLEC4E mRNA expression, Mincle immunofluorescence staining and hMincledependent NF-κB activation demonstrated the involvement of Mincle in the early immune-triggering mechanism. The present study newly elucidated that the molecular recognition and immune-triggering mechanism of K. septempunctata are associated with Mincle on human intestinal epithelial cells. [BMB Reports 2020; 53(9): 478-483].

Purpose of Review: To review recent evidence on the association of urticaria and the gut diseases, focusing on the roles of chronic inflammation with or without Helicobacter pylori (H. Pylori) infection., Recent Findings: The connection between the gut and urticaria has been discussed for a long time. Some publications have shown that H. pylori can induce chronic spontaneous urticaria (CSU). Recently, it was reported that upper gastrointestinal inflammatory disorders can cause CSU and trigger exacerbations independently of H. pylori., Summary: Gastritis and especially H. pylori-induced gastritis has been implicated as potential trigger of CSU. Chronic parasite infection and inflammation of the gut are relevant comorbidities and also potential inducing factors for the development of urticaria.

The Coronavirus disease 2019 (COVID-19) pandemic has killed over two hundred thousand people by end of April, 2020. America and Europe top in deaths from COVID-19 whereas the numbers are lower in Africa for unclear reasons. Emerging evidence suggests the role of hyperactive immune responses characterised by high pro-inflammatory cytokines in severe cases of COVID-19 and deaths. In this perspective, we explore the possible factors that may contribute to mild inflammatory responses in some cases of COVID-19 by focusing on immune education, parasites, sex hormones and chronic diseases, as well as genetic tolerance. To build our perspective, evidence is also extracted from wild rodents due to their multi-tasking immune responses as a result of constant exposure to pathogens., Competing Interests: The author declares no competing interests., (© Samuel Munalula Munjita et al.)

The triggering receptor expressed on myeloid cells 1 (TREM-1) is a receptor of the innate immune system, expressed mostly by myeloid cells and primarily associated with pro- inflammatory responses. Although the exact nature of its ligands has not yet been fully elucidated, many microorganisms or danger signals have been proposed as inducers of its activation or the secretion of sTREM-1, the soluble form with putative anti-inflammatory effects. In the course of the 20   years since its first description, several studies have investigated the involvement of TREM-1 in bacterial infections. However, the number of studies describing the role of TREM-1 in fungal, viral and parasite-associated infections has only increased in the last few years, showing a diverse contribution of the receptor in these scenarios, with beneficial or detrimental activities depending on the context. Therefore, this review aims to discuss how TREM-1 may influence viral, fungal and parasitic infection outcomes, highlighting its potential as a therapeutic target and biomarker for diagnosis and prognosis of non-bacterial infectious diseases.

Recently, the incidence of infectious diseases continues to decline in many developed countries; however, the incidence of autoimmune diseases and allergic asthma appears a tendency towards a rise over years. "Hygiene hypothesis" provides new insights into the treatment of autoimmune disorders and allergic diseases based on parasitic infections. Increasing evidence shows that parasitic infections may effectively inhibit the development of diabetes, multiple sclerosis, inflammatory bowel disease, rheumatoid arthritis and allergic asthma. There are complex mechanisms underlying the relationship between parasitic infections and "hygiene hypothesis", among which regulatory T (Treg) cells and Th17 cells are becoming a hot topic of research. This paper reviews the progresses in the research on the relationship between parasitic infections and "hygiene hypothesis", and summarizes the roles of Treg cells and Th17 cells in the interplay between parasitic infections and "hygiene hypothesis".

Many parasitic infections stimulate antibody responses in their mammalian hosts. The ability of these antibodies to protect against disease varies markedly. Research has revealed that functional properties of antibodies determine their role in protection against parasites. Investigations of antibodies against Plasmodium spp. have demonstrated a variety of functional activities, ranging from invasion inhibition and parasite growth inhibition to antibody-dependent cellular phagocytosis and antibody-dependent cellular cytotoxicity. These activities have been demonstrated with a large variety of parasite molecules at multiple life cycle stages, highlighting the importance of functional antibody responses in malaria. Other parasitic infections have not yet been investigated in similar detail, but these mechanisms are likely to operate in nonmalarial parasitic infections as well. In this report, we review data on the role of functional antibody responses in protection from parasitic infections, highlighting discoveries in malaria, a parasite for which our knowledge base is the most advanced., (© 2020 Australian and New Zealand Society for Immunology Inc.)

The gastric bacterium Helicobacter pylori efficiently evades innate immune detection and persistently colonizes its human host. Understanding the genetic determinants that H. pylori uses to establish and maintain persistence, along with their cellular targets, is key to our understanding of the pathogenesis of this extraordinarily successful bacterial colonizer of the human stomach. This review highlights recent advances in elucidating innate immune recognition of H. pylori, its interactions with myeloid cells and the consequences that this very local infection has for immune responses at extragastric sites in models of allergy, autoimmunity and parasitic infection. The human-specific, gram-negative gastric colonizer and carcinogen H. pylori represents the prototype of a persistent bacterial pathogen. It is transmitted during early childhood, typically from mother to infant, and is believed to persist in its human host from the cradle to the grave. The tremendous success of H. pylori in infecting and colonizing half of the world's population, and in continuously accompanying humans since they migrated out of Africa over 60000 years ago, can largely be attributed to its ability to manipulate the host immune system to its own advantage, and to thereby ensure its own persistence and chronicity. In his final years as an active PI, Stanley Falkow increasingly recognized the need to understand bacterial persistence strategies as a prerequisite of understanding the pathogenesis of chronic bacterial infections, and, inspired in large part by Denise Monack's work on Salmonella persistence, many of our discussions at the time revolved around this topic. Multiple labs have since made important contributions to our understanding of innate immune detection of H. pylori, the types and polarization of adaptive immune responses that ensue, the ability of H. pylori to skew such immune responses to its advantage, and its ability to manipulate the host immune system with far-reaching, even systemic consequences. This review attempts to cover some of these topics, with a particular focus on the most recent contributions by researchers in the field., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Macrophages are important members of innate immunity and play an extremely important role in the host defense against pathogenic infections, tumors, and allergic diseases. Macrophages have a high degree of plasticity, and may be polarized into classical activated macrophages (M1 macrophages) and alternative activated macrophages (M2 macrophages) under the stimulation of different environments. M1 macrophages are found to promote inflammatory responses, which facilitates the clearance of pathogens, while M2 macrophages may inhibit inflammatory responses, which facilitates the survival and reproduction of pathogens. This review summarizes the role of macrophage polarization in parasitic infections, so as to provide insights into the prevention and treatment of parasitic diseases.

Accurate and cost-effective identification of areas where co-endemic infections occur would enable public health managers to identify opportunities for implementation of integrated control programs. Dried blood spots collected during cross-sectional lymphatic filariasis surveys in coastal Kenya were used for exploratory integrated detection of IgG antibodies against antigens from several parasitic infections ( Wuchereria bancrofti , Schistosoma mansoni , Plasmodium spp., Ascaris lumbricoides , and Strongyloides stercoralis ) as well as for detection of responses to immunizing agents used against vaccine-preventable diseases (VPDs) (measles, diphtheria, and tetanus) using a multiplex bead assay (MBA) platform. High heterogeneity was observed in antibody responses by pathogen and antigen across the sentinel sites. Antibody seroprevalence against filarial antigens were generally higher in Ndau Island ( P < 0.0001), which also had the highest prevalence of filarial antigenemia compared with other communities. Antibody responses to the Plasmodium species antigens circumsporozoite protein (CSP) and merozoite surface protein-1 (MSP-1) 19 were higher in Kilifi and Kwale counties, with Jaribuni community showing higher overall mean seroprevalence ( P < 0.0001). Kimorigo community in Taita-Taveta County was the only area where antibody responses against S. mansoni Sm25 recombinant antigen were detected. Seroprevalence rates to Strongyloides antigen NIE ranged between 3% and 26%, and there was high heterogeneity in immune responses against an Ascaris antigen among the study communities. Differences were observed between communities in terms of seroprevalence to VPDs. Seroprotection to tetanus was generally lower in Kwale County than in other counties. This study has demonstrated that MBA holds promise for rapid integrated monitoring of trends of infections of public health importance in endemic areas.

Introduction: Over 300 species of parasites can possibly be passed on humans. Most of the parasitic infections are defined based on their pathogenicity; however, some positive effects of a parasite existence within the human body have recently been suggested. Beneficial outcomes of parasite infections might result from the production and release of metabolites, modification of host immune response or products uptake of the host., Objective: The aim of the study was a comprehensive analysis of a wide range of effects of parasites on the human body, including an overview of the toxic and positive effects., State of Knowledge: In the light of the latest research presenting the unconventional use of parasites in medicine, the widely understood of their impact on the human body can also be considered in a positive context. Clinical cases from diseases caused by the toxic effects of parasites, as described in recent years, indicate that the problem of parasitic infections still persists. Despite a great deal of knowledge about the toxic effects of parasites on the human organism and, above all, despite the improvement in sanitary conditions, there is a resurgence of parasitic infections, as evidenced, e.g. by the examples presented in this review., Conclusions: The examples of positive effects of parasites presented so far give hope for the future in terms of fighting many diseases for which pharmacological treatment has not yet brought a positive effect. A better understanding of those processes might lead to the development of new methods of unconventional medical treatment.

Parasites have evolved various mechanisms to favor infection of their hosts and enhance the success of the infection. In this respect, time-of-day effects were found during the course of parasitic infections, which can be caused or controlled by circadian rhythms in the physiology of their vertebrate hosts. These include circadian clock-controlled rhythms in metabolism and in immune responses. Conversely, parasites can also modulate their hosts' behavioral and cellular rhythms. Lastly, parasites themselves were in some cases shown to possess their own circadian clock mechanisms, which can influence their capacity to infect their hosts. A better knowledge of the circadian regulation of host-parasite interactions will help in designing new preventive and therapeutic strategies for parasitic diseases., (Copyright © 2019 Carvalho Cabral, Olivier and Cermakian.)

The mammalian immune system has evolved the capacity to detect and destroy tumor cells. Tumors utilize multiple strategies to evade host immune surveillance, including the induction of the checkpoint molecules cytotoxic T lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) to suppress antitumor immunity. Pharmacologic blockade of these molecules with checkpoint inhibitors (CPIs) restores T cell function and prolongs survival in patients with various malignancies. Emerging evidence suggests that the same checkpoint pathways may play a crucial role during infections. Indeed, CPIs appear promising as immunotherapeutic agents in infectious diseases, although their efficacy varies depending on pathogen-, cell-, and organ-specific factors. More research will be necessary to clarify the effects and safety of CPIs on clinically relevant outcomes of human infection., (Published by Elsevier Ltd.)

Globally, diseases transmitted by arthropod vectors, such as mosquitoes, remain a major cause of morbidity and mortality [1]. The defense responses of mosquito and other arthropod vectors against parasites are important for understanding disease transmission dynamics and for the development of novel disease-control strategies. Consequently, the mechanisms by which mosquitoes resist parasitic infection (e.g., immune-mediated killing) have long been studied [2, 3]. However, the ability of mosquitoes to ameliorate the negative fitness consequences of infection through tolerance mechanisms (e.g., tissue repair) has been virtually ignored (but see [4, 5]). Ignoring parasite tolerance is especially taxing in vector biology because unlike resistance, which typically reduces vectorial capacity, tolerance is expected to increase vectorial capacity by reducing parasite-mediated mortality without killing parasites [6], contributing to the recurrent emergence of vector-borne diseases and its stabilization and exacerbation. Despite its importance, there is currently no evidence for the evolution of tolerance in natural mosquito populations. Here, we use a common-garden experimental framework to measure variation in resistance and tolerance to dog heartworm (Dirofilaria immitis) between eight natural Aedes albopictus mosquito populations representing areas of low and high transmission intensity. We find significant inter-population variation in tolerance and elevated tolerance where transmission intensity is high. Additionally, as expected, we find that increased tolerance is associated with higher vectorial capacity. Consequently, our results indicate that high transmission intensity can lead to the evolution of more competent disease vectors, which can feed back to impact disease risk., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

We investigated the impact of helminths and malaria infection on Kaposi's sarcoma associated herpesvirus (KSHV) seropositivity, using samples and data collected from a cluster-randomised trial of intensive versus standard anthelminthic treatment. The trial was carried out in 2012 to 2016 among fishing communities on Lake Victoria islands in Uganda. Plasma samples from 2881 participants from two household surveys, the baseline (1310 participants) and the final (1571 participants) surveys were tested for KSHV IgG antibody responses to K8.1 and ORF73 recombinant proteins using ELISA. The baseline survey was carried out before the trial intervention while the final survey was carried out after three years of the trial intervention. Additionally, a subset sample of 372 participants from the final survey was tested for IgE, IgG and IgG4 antibody concentrations to S. mansoni adults worm antigen (SWA) and S. mansoni egg antigen (SEA) using ELISA. Infection by helminths (S. mansoni, N. americanus, T. trichiura and S. stercoralis) was diagnosed using real-time PCR, urine circulating cathodic antigen (CCA) and stool microscopy (Kato-Katz method) while malaria infection was diagnosed using microscopy. We analysed the relationship between helminth and malaria infections and KSHV seropositivity using regression modelling, allowing for survey design. At baseline, 56% of the participants were male while 48% of the participants were male in the final survey. The most prevalent helminth infection was S. mansoni (at baseline 52% and 34% in the final survey by microscopy, 86% by CCA and 50% by PCR in the final survey). KSHV seropositivity was 66% (baseline) and 56% (final survey) among those 1-12 years and >80% in those 13+ years in both surveys; malaria parasitaemia prevalence was 7% (baseline) and 4% (final survey). At baseline, individuals infected with S. mansoni (detected by microscopy) were more likely to be KSHV seropositive (aOR = 1.86 (1.16, 2.99) p = 0.012) and had higher anti-K8.1 antibody levels (acoefficient = 0.03 (0.01, 0.06) p = 0.02). In the final survey, S. mansoni (by microscopy, adjusted Odds Ratio (aOR = 1.43 (1.04-1.95), p = 0.028) and malaria parasitaemia (aOR = 3.49 (1.08-11.28), p = 0.038) were positively associated with KSHV seropositivity. Additionally, KSHV seropositive participants had higher S. mansoni-specific IgE and IgG antibody concentrations in plasma. Furthermore, HIV infected individuals on cART were less likely to be KSHV seropositive compared to HIV negative individuals (aOR = 0.46 (0.30, 0.71) p = 0.002). Schistosoma species skew the immune response towards Th2 and regulatory responses, which could impact on KSHV reactivation if co-infected with both organisms., Competing Interests: The authors have declared that no competing interests exist.

As a cytoplasmic protein tyrosine kinase, Bruton's tyrosine kinase (Btk) is widely considered as a vital kinase in many aspects of different physiologic processes. It is engaged in many important signalling pathways related to the immune response, such as the B cell receptor pathway, pattern-recognition receptor pathway, and triggering receptor expressed on myeloid cell pathway. Recent studies have increasingly focused on the important role of Btk in various inflammatory diseases, which are related to Btk expression in myeloid innate immune cells, such as macrophages, dendritic cells and neutrophils. Although some investigations have explored the role of Btk in microbial infections, many aspects remain elusive, and some of the results are opposite and controversial. Considering the complicated and multiple roles of Btk in the immune system, we summarized the engagement of Btk signalling in various pathogenic microorganism infections, the possible mechanisms involved and its therapeutic potential in the control of infectious diseases., (© 2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.)

Eosinophilic dermatoses are a heterogeneous group of diseases, characterized by an eosinophil-rich infiltrate and/or degranulation of eosinophils. Blood eosinophilia may be an associated feature. Typical, albeit not specific histological findings include 'flame figures', which are caused by the accumulation of cationic proteins released by eosinophils and subsequent collagen denaturation. "Classic" eosinophilic dermatoses include eosinophilic cellulitis (Wells syndrome), granuloma faciale, eosinophilic fasciitis (Shulman syndrome) and eosinophilic folliculitis (Ofuji disease). In addition, there is a multitude of skin diseases that present with varying degrees of eosinophilic infiltration. These include atopic dermatitis, bullous pemphigoid, urticaria, allergic contact dermatitis, prurigo nodularis, arthropod bite reaction, parasitic infections, and drug hypersensitivity. Even though these disorders share a common characteristic (tissue eosinophilia), they differ greatly in their clinical presentation., (© 2019 Deutsche Dermatologische Gesellschaft (DDG). Published by John Wiley & Sons Ltd.)

Early diagnosis and treatment of parasitic diseases are indispensable to combat parasites mediated morbidity and mortality in humans and animals. Mammalian sourced antibodies are being successfully used in immunotherapy and immunoassays. However, their increased conservation amongst mammals, involves them in unnecessary interaction and immune mediated pathologies, obstructing their applications in certain approaches in immunoassays. Further, the high production cost and difficulty to achieve high and stable antibody titer hampers their utility for therapeutic purposes. In recent years, chicken egg yolk immunoglobulin, termed as immunoglobulin Y (IgY) has attracted noticeable consideration since it poses greater advantages than mammalian IgG including high yield, low cost and convenience. IgY has unique properties which are being exploited in different aspects for its applications in research, diagnosis and therapy. This review gives an overview of the research outcomes pertaining to chicken IgY as diagnostics and therapeutics in parasitology., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Parasitic infections are responsible for significant morbidity and mortality throughout the world. Management strategies rely primarily on antiparasitic drugs that have side effects and risk of drug resistance. Therefore, novel strategies are needed for treatment of parasitic infections. Host-directed therapy (HDT) is a viable alternative, which targets host pathways responsible for parasite invasion/survival/pathogenicity. Recent innovative combinations of genomics, proteomics and computational biology approaches have led to discovery of several host pathways that could be promising targets for HDT for treating parasitic infections. Herein, we review major advances in HDT for parasitic disease with regard to core regulatory pathways and their interactions.