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The immune system interacts with many nominal 'danger' signals, endogenous danger‐associated (DAMP), exogenous pathogen (PAMP) and allergen (AAMP)‐associated molecular patterns. The immune context under which these are received can promote or prevent immune activating or inflammatory mechanisms and may orchestrate diverse immune responses in allergy and cancer. Each can act either by favouring a respective pathology or by supporting the immune response to confer protective effects, depending on acuity or chronicity. In this Position Paper under the collective term danger signals or DAMPs, PAMPs and AAMPs, we consider their diverse roles in allergy and cancer and the connection between these in AllergoOncology. We focus on their interactions with different immune cells of the innate and adaptive immune system and how these promote immune responses with juxtaposing clinical outcomes in allergy and cancer. While danger signals present potential targets to overcome inflammatory responses in allergy, these may be reconsidered in relation to a history of allergy, chronic inflammation and autoimmunity linked to the risk of developing cancer, and with regard to clinical responses to anti‐cancer immune and targeted therapies. Cross‐disciplinary insights in AllergoOncology derived from dissecting clinical phenotypes of common danger signal pathways may improve allergy and cancer clinical outcomes. [ABSTRACT FROM AUTHOR]

Objectives The immune trypanolysis test ( TL) is an accurate sero-diagnostic tool increasingly implemented for sleeping sickness medical surveillance, but it is restricted to the reference laboratories. To facilitate storage and transport of the test specimen, we developed a protocol for the examination of blood spotted on filter paper ( TL-fp) that can be stored and shipped at ambient temperature. We compared its performance with the classical TL on plasma ( TL-pl) that needs to be kept frozen until use. Methods The study was conducted in active foci of the Republic of Guinea. In total, 438 specimens from treated and untreated sleeping sickness patients and serological suspects were tested with both methods. Result TL-fp gave significantly less positive results than TL-pl, but all the confirmed sleeping sickness cases were positive with the TL-fp protocol. Conclusion TL-fp appears to offer a good compromise between feasibility and sensitivity to detect currently infected subjects who play a role in the transmission of Trypanosoma brucei gambiense and is useful for contributing to the elimination of gambiense sleeping sickness. [ABSTRACT FROM AUTHOR]

Th2 immunity and allergic immune surveillance play critical roles in host responses to pathogens, parasites and allergens. Numerous studies have reported significant links between Th2 responses and cancer, including insights into the functions of IgE antibodies and associated effector cells in both antitumour immune surveillance and therapy. The interdisciplinary field of AllergoOncology was given Task Force status by the European Academy of Allergy and Clinical Immunology in 2014. Affiliated expert groups focus on the interface between allergic responses and cancer, applied to immune surveillance, immunomodulation and the functions of IgE-mediated immune responses against cancer, to derive novel insights into more effective treatments. Coincident with rapid expansion in clinical application of cancer immunotherapies, here we review the current state-of-the-art and future translational opportunities, as well as challenges in this relatively new field. Recent developments include improved understanding of Th2 antibodies, intratumoral innate allergy effector cells and mediators, IgE-mediated tumour antigen cross-presentation by dendritic cells, as well as immunotherapeutic strategies such as vaccines and recombinant antibodies, and finally, the management of allergy in daily clinical oncology. Shedding light on the crosstalk between allergic response and cancer is paving the way for new avenues of treatment. [ABSTRACT FROM AUTHOR]

In this paper, we study a delayed HIV infection model with nonmonotonic immune response and perform stability and bifurcation analysis. Our results show that the delayed HIV infection system with nonmonotonic immune response has bistability and stable periodic solution appear. We find that both the uninfected and immune-free equilibria are globally asymptotically stable under certain conditions which are not affected by time delay. However, the time delay makes one immune equilibrium always unstable for τ ≥ 0 and also makes another immune equilibrium appear stability switches; meanwhile, the system will exhibit local Hopf bifurcation, global Hopf bifurcation, and saddle-node-Hopf bifurcation. Numerical simulations are carried out to verify our results. [ABSTRACT FROM AUTHOR]

Atopic dermatitis ( AD) is a clinically defined, highly pruritic, chronic inflammatory skin disease of children and adults. The diagnosis is made using evaluated clinical criteria. Disease activity is best measured with a composite score assessing both objective signs and subjective symptoms, such as SCORAD. The management of AD must consider the clinical and pathogenic variabilities of the disease and also target flare prevention. Basic therapy includes hydrating topical treatment, as well as avoidance of specific and unspecific provocation factors. Anti-inflammatory treatment of visible skin lesions is based on topical glucocorticosteroids and the topical calcineurin inhibitors tacrolimus and pimecrolimus. Topical calcineurin inhibitors are preferred in sensitive locations. Tacrolimus and mid-potent steroids are proven for proactive therapy, which is long-term intermittent anti-inflammatory therapy of the frequently relapsing skin areas. Systemic anti-inflammatory or immunosuppressive treatment is indicated for severe refractory cases. Biologicals targeting key mechanisms of the atopic immune response are promising emerging treatment options. Microbial colonization and superinfection may induce disease exacerbation and can justify additional antimicrobial treatment. Systemic antihistamines (H1R-blockers) may diminish pruritus, but do not have sufficient effect on lesions. Adjuvant therapy includes UV irradiation, preferably UVA1 or narrow-band UVB 311 nm. Dietary recommendations should be patient specific and elimination diets should only be advised in case of proven food allergy. Allergen-specific immunotherapy to aeroallergens may be useful in selected cases. Psychosomatic counselling is recommended to address stress-induced exacerbations. 'Eczema school' educational programmes have been proven to be helpful for children and adults. [ABSTRACT FROM AUTHOR]

The article offers information on several research articles published in the "Asian Journal of Ecotoxicology." Topics discussed include the bioaccumulative effects of halogenated flame retardants (HFRs) in catfish and pigeon; analysis of differentially expressed microRNAs using microarrays in lung tissue of mouse induced by particulate matter; and the effect of cadmium (Cd) exposure on antioxidant and immune response in the liver.

Background: Sexual dimorphism is observed in the occurrence, course, and severity of human disease. The difference in immune response between males and females can in part be attributed to sexual genotype. However, immunological differences can also be explained by endocrine–immune interactions. Specifically, androgens possess the ability of directly modulating the development and function of immune cells. Although androgens generally contribute to immunosuppressive effects, this is not necessarily always the case. Aim: The aim of the review is to uncover the role of androgens in shaping the innate immune response. Material & Methods: Authors included papers in this review which discussed the impact of androgens on specific innate immune cells. Results: Androgens modulate the innate immune response through various mechanisms. However, there is conflicting evidence in the literature regarding the interplay betwen androgens and the innate immune system. Discussion: Conflicting evidence presented in this review could in part be explained by the limitations present in interpreting results. Conclusion: This review is of great importance for our understanding of occurence and mechanism of human inflammatory disease. [ABSTRACT FROM AUTHOR]

In tropical and subtropical regions of the world, leishmaniasis is endemic and causes a range of clinical symptoms in people, from severe tegumentary forms (such as cutaneous, mucocutaneous, and diffuse leishmaniasis) to lethal visceral forms. The protozoan parasite of the genus Leishmania causes leishmaniasis, which is still a significant public health issue, according to the World Health Organization 2022. The public's worry about the neglected tropical disease is growing as new foci of the illness arise, which are exacerbated by alterations in behavior, changes in the environment, and an enlarged range of sand fly vectors. Leishmania research has advanced significantly during the past three decades in a few different avenues. Despite several studies on Leishmania, many issues, such as illness control, parasite resistance, parasite clearance, etc., remain unresolved. The key virulence variables that play a role in the pathogenicity‐host‐pathogen relationship of the parasite are comprehensively discussed in this paper. The important Leishmania virulence factors, such as Kinetoplastid Membrane Protein–11 (KMP‐11), Leishmanolysin (GP63), Proteophosphoglycan (PPG), Lipophosphoglycan (LPG), Glycosylinositol Phospholipids (GIPL), and others, have an impact on the pathophysiology of the disease and enable the parasite to spread the infection. Leishmania infection may arise from virulence factors; they are treatable with medications or vaccinations more promptly and might greatly shorten the duration of treatment. Additionally, our research sought to present a modeled structure of a few putative virulence factors that might aid in the development of new chemotherapeutic approaches for the treatment of leishmaniasis. The predicted virulence protein's structure is utilized to design novel drugs, therapeutic targets, and immunizations for considerable advantage from a higher understanding of the host immune response. [ABSTRACT FROM AUTHOR]

In this paper, we develop a diffusive and delayed hepatitis B virus (HBV) infection model, which incorporates both virus‐to‐cell and cell‐to‐cell transmissions along with cytotoxic T lymphocyte (CTL) immune response. Two threshold parameters ℜ0$$ {\mathfrak{\Re}}_0 $$ (basic reproduction number) and ℜ1$$ {\mathfrak{\Re}}_1 $$ (immune response reproduction number) are defined, which determine the dynamic behavior of the model. Employing the approach of Lyapunov functionals, we show that the infection‐free steady state is globally asymptotically stable when ℜ0≤1$$ {\mathfrak{\Re}}_0\le 1 $$; the immune‐free infected steady state is globally asymptotically stable when ℜ1≤1<ℜ0$$ {\mathfrak{\Re}}_1\le 1<{\mathfrak{\Re}}_0 $$; and the immune‐present steady state is globally asymptotically stable when ℜ0>1,ℜ1>1$$ {\mathfrak{\Re}}_0>1,{\mathfrak{\Re}}_1>1 $$, and φ(I)=I$$ \varphi (I)=I $$. We perform the sensitivity and uncertainly analysis on ℜ0$$ {\mathfrak{\Re}}_0 $$ with respect to parameters and find that the most important parameter that drives the HBV infection is the mortality of HBV DNA capsids. Moreover, the theoretical results are supported with numerical simulations. [ABSTRACT FROM AUTHOR]

Summary: In the 2 years since the COVID‐19 pandemic was officially declared, science has made considerable strides in understanding the disease's pathophysiology, pharmacological treatments, immune response, and vaccination, but there is still much room for further advances, especially in comprehending its relationship with obesity. Science has not yet described the mechanisms that explain how obesity is directly associated with a poor prognosis. This paper gathers all published studies over the past 2 years that have described immune response, obesity, and COVID‐19, a historical and chronological record for researchers and the general public alike. In summary, these studies describe how the cytokine/adipokine levels and inflammatory markers, such as the C‐reactive protein, are associated with a higher body mass index in COVID‐19‐positive patients, suggesting that the inflammatory background and immune dysregulation in individuals with obesity may be expressed in the results and that adiposity may influence the immune response. The timeline presented here is a compilation of the results of 2 years of scientific inquiry, describing how the science has progressed, the principal findings, and the challenges ahead regarding SARS‐CoV‐2, COVID‐19, and emerging variants, especially in patients with obesity. [ABSTRACT FROM AUTHOR]

Immunogenic cell death (ICD) arises when cells are under stress, and their membranes are damaged. They release damage‐associated molecular patterns (DAMPs) that stimulate and drive the type and magnitude of the immune response. In the presence of an antigen, DAMPs ride the longevity and efficacy of antigen‐specific immunity. Yet, no tool can induce the controlled ICD with predictable results. A peptide‐based tool, [II], is designed that aggregates in the cell and causes cell membrane damage, generates ICD and DAMPs release on various cell types, and hence can act as an adjuvant. An influenza vaccine is prepared by combining [II] with influenza hemagglutinin (HA) subunit antigens. The results show that [II] induced significantly higher HA‐specific immunoglobulin G1 (IgG1) and IgG2a antibodies than HA‐only immunized mice, while the peptide itself did not elicit antibodies. This paper demonstrates the first peptide‐aggregation induced immunogenic rupture (PAIIR) approach as a vaccine adjuvant. PAIIR is a promising adjuvant with a high potential to promote universal protection upon influenza HA vaccination. [ABSTRACT FROM AUTHOR]

In this paper, the dynamics of stochastic human T‐cell leukemia virus type I (HTLV‐I) infection model with cytotoxic T lymphocyte (CTL) immune response is investigated. First, we show that the stochastic model exists as a unique positive global solution originating from the positive initial value. Second, we demonstrate that the stochastic model is stochastically permanent and stochastically ultimately bounded for any positive initial value. Third, we establish sufficient conditions for the existence of ergodic stationary distribution of the stochastic model. Fourth, the threshold R0∗ between extinction and persistence of the virus is obtained. Finally, numerical simulations are carried out to illustrate the theoretical results. [ABSTRACT FROM AUTHOR]

Coronavirus disease 2019 (COVID‐19), can present with a wide spectrum of severity. Elderly patients with cardiac, pulmonary and metabolic comorbidities are more likely to develop the severe manifestations of COVID‐19, which are observed in less than 5% of the pediatric patients. Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) is able to induce an immune impairment and dysregulation, finally resulting in the massive release of inflammatory mediators, strongly contributing to the pulmonary and systemic manifestations in COVID‐19. In children, the immune dysregulation following SARS‐CoV‐2 can also be responsible of a severe disease phenotype defined as multisystem inflammatory syndrome in children. As the immune system undergoes a complex process of maturation from birth to adult age, differences in the immune and inflammatory response could have a significant impact in determining the spectrum of severity of COVID‐19. Indeed, children show a higher ability to respond to viral infections and a reduced baseline pro‐inflammatory state compared with elderly patients. Age and comorbidities contribute to disease severity through immune‐mediated mechanisms, since they are associated with a chronic increase of pro‐inflammatory mediators, and cause an enhanced susceptibility to develop an immune dysregulation following SARS‐CoV‐2 infection. Also the expression of ACE2, the receptor of SARS‐CoV‐2, varies with age, and is linked to the immune and inflammatory response through a complex, and not completely elucidated, network. This paper reviews the peculiar immunopathogenic aspects of COVID‐19, with a focus on the differences between adult and pediatric patients. [ABSTRACT FROM AUTHOR]

Recent researches show that virus‐to‐cell infection and cell‐to‐cell transmission are two HIV infection modes. In this paper, we propose a delayed HIV infection model including both virus‐to‐cell infection and cell‐to‐cell transmission and cytotoxic T lymphocyte immune response. The time delay describes the phenomenon between viral entry and viral production. We show the nonnegativity and boundedness of solution, obtain the steady states, and prove local asymptotic stability of the steady states. Then the optimal control problem with antiretroviral therapy and pharmacological delay is posed. We establish and analyze two types of objective functions: one is linear control and the other is quadratic control. Numerical simulations have been performed to verify the stability of steady states and show the optimal control strategies and the effects of control on cells concentration by Matlab and Lingo. [ABSTRACT FROM AUTHOR]

As an oncogene, myelocytomatosis oncogene (MYC) is implicated in the concept of "oncogene addiction," where switching off the oncogene leads to the cell cycle arrest and cell differentiation. However, recent data suggest that MYC also controls the establishment of the tumour microenvironment and that "oncogene addiction" actually has a strong immune background. Evaluation of the MYC role in the immunoediting process led to the speculation that cancer just uses and distorts the physiological mechanism by which MYC normally prevents rapidly proliferating cells from the elicitation of an autoimmune response. Concordantly, elevated levels of MYC and induction of immunosuppressive molecules are observed during the processes of growth and development, tissue repair, placenta development, and so forth, implying that MYC may be involved in saving regular physiologically proliferating cells from the immune system attack. Even more, a growing body of evidence suggests MYC involvement in the shaping of the adaptive immune response, immunological memory development, and establishment of immunotolerance. This paper offers an overview of MYC actions in the context of modulation of the immune response in pathological and physiological conditions. The determination of such a new role for a well‐known oncogene opens new perspectives in biomedicine, and consequently, in the treatment of various pathological conditions. [ABSTRACT FROM AUTHOR]

The article presents a list of forthcoming papers on immunology. Some of the papers include Cross-Linking of Neutrophil CD11b Results in Rapid Cell Surface Expression of Molecules Required for Antigen Presentation and T-Cell Activation," "Various Members of the Toll-Like Receptor Family Contribute to the Innate Immune Response of Human Epidermal Keratinocytes," "Identification and Characterisation of a Functional, Alternatively Spliced TLR7 and Genomic Disruption of TLR8 in Chickens," and "Introduction of Human Papillomavirus Type 16-Specific Immunologic Responses in a Normal and an HPV Infected Populations."

In this paper, a periodic stochastic human immunodeficiency virus (HIV) model with distributed delay and cytotoxic T lymphocytes (CTL) immune response is investigated. First, by It ô's formula, we show that the solution with any positive initial value is global and positive. Then, by the stochastic comparison theorem, we obtain the sufficient conditions guaranteeing the existence and global attractivity of infection‐free periodic solution. Furthermore, we discuss the existence of the infective periodic solution by Has'minskii theory. Finally, numerical examples are given to illustrate the results. [ABSTRACT FROM AUTHOR]

Neutrophil activity, including trapping of damage‐associated molecular patterns by neutrophil extracellular traps (NETs), is an important response to microbial infection. Most activated neutrophils commit to apoptosis and are removed by activated macrophages in the process of efferocytosis. Improper clearance of apoptotic neutrophils often causes an unnecessary and exaggerated immune response and subsequent chronic inflammation. Effective macrophage mobility toward activated neutrophils, which is triggered by binding of 'find‐me' signals to receptors such as P2Y2, is a crucial step for the timely clearance of apoptotic neutrophils. In this paper, we investigated the effect of 1‐palmitoyl‐2‐linoleoyl‐3‐acetyl‐rac‐glycerol (PLAG) on efferocytosis and the underlying molecular mechanisms. In a coculture of apoptotic neutrophils with macrophages, PLAG treatment increased levels of efferocytosis of apoptotic neutrophils. PLAG induced faster translocation of P2Y2 from lipid rafts to nonlipid raft plasma membrane domains in macrophages. This repositioning of P2Y2 enables the polarization of the cytoskeleton by association of the receptor with cytoskeletal proteins such as α‐tubulin and actin to improve the mobility of macrophages. The formation of vesicular, chylomicron‐like structures by PLAG was a prerequisite for the induction of this macrophage activity, as none of these effects was seen when the vesicle receptor GPIHBP1 was absent. Taken together, these data showed that PLAG is a powerful immune resolvent that triggers the prompt clearance of apoptotic neutrophils by enhanced efferocytosis activity. PLAG could therefore be an effective lipid‐based efferocytosis enhancer for use as a therapeutic drug to prevent inflammatory disease caused by uncontrolled immune responses. [ABSTRACT FROM AUTHOR]

Direct cell‐to‐cell transmission of HIV‐1 is a more efficient means of virus infection than virus‐to‐cell transmission. In this paper, we incorporate both these transmissions into an HIV‐1 virus model with nonlinear general incidence rate, intracellular delay, and cytotoxic T lymphocyte (CTL) immune responses. This model admits three types of equilibria: infection‐free equilibrium, CTL‐inactivated equilibrium, and CTL‐activated equilibrium. By using Lyapunov functionals and LaSalle invariance principle, it is verified that global threshold dynamics of the model can be explicitly described by the basic reproduction numbers. [ABSTRACT FROM AUTHOR]

Bladder cancer is one of the most common malignant diseases in the urinary system and a highly aggressive neoplasm. The prognosis is not favorable usually, and its evolution for particular patients is very difficult to find out. In this paper, we propose a dynamic mathematical model that describes the bladder tumor growth and the immune response evolution. This model is customized for a single patient, determining appropriate model parameter values via model calibration. Due to the uncertainty of the tumor evolution, using the calibrated model parameters, we predict the tumor size and the immune response evolution over the next few months assuming three different scenarios: favorable, neutral, and unfavorable. In the former, it is not expected any trace of the cancer in the middle of September 2018 (after 16 mo). In the neutral scenario, at the same date, a 7‐ to 8‐mm tumor is expected. In the worst case, a 40‐mm tumor is expected. The patient was cited on 10 September 2018 to check the tumor size, and according to the doctors, there was no sign of recurrence. It seems that we are in the favorable scenario. The patient will be called again for follow‐up in mid‐2019. [ABSTRACT FROM AUTHOR]

In this paper, we proposed a multidelayed in‐host HIV model to represent the interaction between human immunodeficiency virus and immune response. One delay was considered to incorporate the time required by the virus for various intracellular events to make a host cell productively infective, and the second delay was introduced to take into account the time required for adaptive immune system to respond against infection. We extensively analyzed this multidelayed model analytically and numerically. We show that delay may have both destabilizing and stabilizing effects even when the system contains a single immune response delay. It happens when there exists two sequences of critical values of this delay. If the system starts with stable state in absence of delay, then the smallest value of these critical delays causes instability and the next higher value causes stability. The system may also show stability switching for different values of the virus replication factor. These results demonstrate the possible reasons of intrapatients and interpatients variability of CD4+ T cells and virus counts in HIV‐infected patients. [ABSTRACT FROM AUTHOR]

T‐bet is a major transcription factor increasing inflammatory responses in the immune system. Recently, it has been shown that this factor leads to inflammation in cardiovascular disease (CVD). In this study, we examine the dual role of T‐bet in inducing and suppressing inflammatory reactions as well as angiogenesis induction due to inflammatory cytokines in CVD. Relevant literature was identified by a Pubmed search (1992–2018) of English‐language papers using the terms "T‐bet," "Cardiovascular disease," "Immune response," and "Angiogenesis." Although T‐bet causes differentiation of Th1 cells and activation of immune cells such as NK and DC, it suppresses inflammatory responses and replaces damaged vessels with new ones by activating regulatory T‐cells and stimulating angiogenesis. It can be stated that T‐bet acts as double‐edged sword. Therefore, the identification of pathways that can increase the function of T‐bet in activating Tregs and inducing angiogenesis might be used as a new therapeutic option in future investigations. HIGHLIGHTS: T‐bet factor plays an essential role in the regulation of immune responses in CVD.T‐bet factor induces angiogenesis through the mediation of inflammatory cytokines.T‐bet can be effective in CVD pathogenesis via interaction with other transcription factors. This manuscript attempts to discuss effect of T‐bet on function of immune cell in cardiovascular disease. Also we evaluation of relationship between T‐bet and angiogenesis by inflammatory cytokine and endothelial progenitor cells. [ABSTRACT FROM AUTHOR]

Summary: Cyclic AMP plays important roles in different physiological processes, including plant defence responses. However, as little information is known on plant enzymes responsible for cAMP production/degradation, studies of cAMP functions have relied, to date, on non‐specific pharmacological approaches. We therefore developed a more reliable approach, producing transgenic Arabidopsis thaliana lines overexpressing the 'cAMP‐sponge' (cAS), a genetic tool that specifically buffers cAMP levels. In response to an avirulent strain of Pseudomonas syringae pv. tomato (PstAvrB), cAS plants showed a higher bacterial growth and a reduced hypersensitive cell death in comparison with wild‐type (WT) plants. The low cAMP availability after pathogen infection delayed cytosolic calcium elevation, as well as hydrogen peroxide increase and induction of redox systems. The proteomic analysis, performed 24 h post‐infection, indicated that a core of 49 proteins was modulated in both genotypes, while 16 and 42 proteins were uniquely modulated in WT and cAS lines, respectively. The involvement of these proteins in the impairment of defence response in cAS plants is discussed in this paper. Moreover, in silico analysis revealed that the promoter regions of the genes coding for proteins uniquely accumulating in WT plants shared the CGCG motif, a target of the calcium‐calmodulin‐binding transcription factor AtSR1 (Arabidopsis thaliana signal responsive1). Therefore, following pathogen perception, the low free cAMP content, altering timing and levels of defence signals, and likely acting in part through the mis‐regulation of AtSR1 activity, affected the speed and strength of the immune response. Significance Statement: This study introduces the use of the cAMP‐sponge as a genetic tool to investigate the role of cAMP in plant immune responses, revealing the complexity of the signal network involved in the establishment of plant resistance against an avirulent strain of Pseudomonas syringae pv. tomato. The decrease in free cAMP content, altering the timing and levels of cytosolic calcium and hydrogen peroxide signals upon pathogen perception, affected the speed and strength of the immune response. [ABSTRACT FROM AUTHOR]

Despite years of intensive research, breast cancer remains the leading cause of death in women worldwide. New technologies including oncolytic virus therapies, virus, and phage display are among the most powerful and advanced methods that have emerged in recent years with potential applications in cancer prevention and treatment. Oncolytic virus therapy is an interesting strategy for cancer treatment. Presently, a number of viruses from different virus families are under laboratory and clinical investigation as oncolytic therapeutics. Oncolytic viruses (OVs) have been shown to be able to induce and initiate a systemic antitumor immune response. The possibility of application of a multimodal therapy using a combination of the OV therapy with immune checkpoint inhibitors and cancer antigen vaccination holds a great promise in the future of cancer immunotherapy. Display of immunologic peptides on bacterial viruses (bacteriophages) is also increasingly being considered as a new and strong cancer vaccine delivery strategy. In phage display immunotherapy, a peptide or protein antigen is presented by genetic fusions to the phage coat proteins, and the phage construct formulation acts as a protective or preventive vaccine against cancer. In our laboratory, we have recently tested a few peptides (E75, AE37, and GP2) derived from HER2/neu proto‐oncogene as vaccine delivery modalities for the treatment of TUBO breast cancer xenograft tumors of BALB/c mice. Here, in this paper, we discuss the latest advancements in the applications of OVs and bacterial viruses display systems as new and advanced modalities in cancer immune therapeutics. This manuscript discusses the latest findings regarding viral vectors designed for fighting breast cancer [ABSTRACT FROM AUTHOR]

Aim: To evaluate the mRNA expression levels of the cytokines interferon‐γ, tumour necrosis factor‐α, interleukin (IL)‐1β, IL‐10, IL‐6, VEGF, and AGT and the chemokine CCL2/MCP‐1 in periapical interstitial fluid associated with root canal infections before and after the reduction of the bacterial load using a cleaning procedure. Methodology: The case group included 11 patients with chronic liver disease, and the control group included 11 healthy patients. Clinical samples were taken from teeth with pulp necrosis. After cleaning and drying the canal, three paper points were introduced into the root canal and passed through the root apex (2 mm) into the periapical tissues for 1 min. The samples were collected immediately after root canal cleaning and 7 days later to characterize those gene expression levels using real‐time PCR. The data were subjected to the Shapiro–Wilk and the Wilcoxon tests. Results: In the control group, significantly increased expression of the pro‐inflammatory cytokines IFN‐γ and TNF‐α was observed in teeth with restrained bacterial loads (day 7) (P < 0.05). Similarly, increased TNF‐α expression was found on day 7 in the liver group (P < 0.05). No differences were observed in the expression levels of the IL‐1β, IL‐10 and, IL‐6, MCP‐1/CCL‐2 and VEGF between the first collection (day 0) and second collection (day 7), over time in either group. Conclusion: Chronic liver disease patients exhibited sufficient immunologic ability showing relatively similar expression levels of cytokines, chemokines and angiogenic factors in periapical samples compared with the responses from no‐chronic liver disease patients. The outcomes of this study suggest that liver impairment did not compromise the periapical immune response. [ABSTRACT FROM AUTHOR]

We study a mathematical model of immune response by T cells where the regulatory T cells (Treg) inhibit interleukin 2 (IL‐2) secretion. We model the suppression of the autoimmune line of T cells after a different line of T cells responded to a pathogen infection. In this paper, we show that if the population of the pathogen responding line of T cells becomes large enough, the competition for IL‐2 and the increase in the death rates may lead to a depletion in the concentration of autoimmune T cells. Provided this lasts for a sufficiently long time, the concentration of autoimmune T cells can be brought down to values inside the basin of attraction of the controlled state, and autoimmunity can be suppressed. [ABSTRACT FROM AUTHOR]

The article lists several papers related to immune system that are to be published in the December 2004 issue of the journal "Immunology." Some of the papers are "Phenotypic and Functional Heterogeneity of Porcine Blood Monocytes and Its Relation With Maturation," by Sonia Chamorro, Concepcion Revilla, Belen Alvarez, Fernando Alonso, Angel Ezquerra, Javier Dominguez; "Influence of Pathological Progression on the Balance Between Cellular and Humoral Immune Responses in Bovine Tuberculosis," Michael Welsh, Rodat Cunningham, David Corbett, R. Martyn Girvin, James McNair, Robin Skuce, David Bryson, John Pollock.

LINKED CONTENT This article is linked to Chanchlani et al papers. To view these articles, visit https://doi.org/10.1111/apt.17170 [ABSTRACT FROM AUTHOR]

In this paper, we propose an improved human T‐cell leukemia virus type 1 infection model with mitotic division of actively infected cells and delayed cytotoxic T lymphocyte immune response. By constructing suitable Lyapunov functional and using LaSalle invariance principle, we investigate the global stability of the infection‐free equilibrium of the system. Our results show that the time delay can change stability behavior of the infection equilibrium and lead to the existence of Hopf bifurcations. Finally, numerical simulations are conducted to illustrate the applications of the main results. [ABSTRACT FROM AUTHOR]

Chemokines are cytokines that are involved in the movement of leukocytes and the occurrence of immune responses. It has recently been noted that these cytokines play a role in the movement of cancer cells to different parts of the body and create a suitable environment [i.e. (pre) metastatic niche] for their growth and proliferation. We studied the role of chemokines in the metastasis of cancer cells, as well as their involvement in the proliferation and growth of these cells. Relevant literature was identified by a PubMed search (2005–2017) of English language papers using the terms ‘chemokine,’ ‘metastasis niche,’ and ‘organotropism.’ Based on the nature of cancer cells, the expression of chemokine receptors on these cells leads to metastasis to various organs, which ultimately causes changes in different signaling pathways. Finally, the targeting of chemokines on cancer cells could prevent the metastasis of cancer cells toward different organs. [ABSTRACT FROM AUTHOR]

Summary: Nosema ceranae is a hot topic in honey bee health as reflected by numerous papers published every year. This review presents an update of the knowledge generated in the last 12 years in the field of N. ceranae research, addressing the routes of transmission, population structure and genetic diversity. This includes description of how the infection modifies the honey bee's metabolism, the immune response and other vital functions. The effects on individual honey bees will have a direct impact on the colony by leading to losses in the adult's population. The absence of clear clinical signs could keep the infection unnoticed by the beekeeper for long periods. The influence of the environmental conditions, beekeeping practices, bee genetics and the interaction with pesticides and other pathogens will have a direct influence on the prognosis of the disease. This review is approached from the point of view of the Mediterranean countries where the professional beekeeping has a high representation and where this pathogen is reported as an important threat. [ABSTRACT FROM AUTHOR]

The immune response against platelets is a complex process involving many aspects of the innate and adaptive immune system. Immune destruction of platelets and megakaryocytes and the thrombocytopenia that ensues can cause different clinically significant haematological disorders such as foetal and neonatal alloimmune thrombocytopenia (FNAIT), transfusion‐induced platelet refractoriness or immune thrombocytopenia (ITP). These conditions are frequently difficult to manage so an understanding of the biological nature of these adverse conditions is critical for an understanding of how to potentially reduce them. Superimposed on these immune platelet attack mechanisms are the immune characteristics of the platelets themselves. This paper will give an overview of how the immune system recognizes platelet antigens and mounts efficient effector mechanism to mediate thrombocytopenia. It will also present evidence to suggest that platelets also play a role in stimulating these responses and suppressing them: a scenario where the ‘prey’ can become the ‘predator’. [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Colman et al papers. To view these articles, visit https://doi.org/10.1111/apt.16733 [ABSTRACT FROM AUTHOR]

In this paper, the diffusion is introduced to an immunosuppressive infection model with delayed antiviral immune response. The direction and stability of Hopf bifurcation are effected by time delay, in the absence of which the positive equilibrium is locally asymptotically stable by means of analyzing eigenvalue spectrum; however, when the time delay increases beyond a threshold, the positive equilibrium loses its stability via the Hopf bifurcation. The stability and direction of the Hopf bifurcation is investigated with the norm form and the center manifold theory. The stability of the Hopf bifurcation leads to the emergence of spatial spiral patterns. Numerical calculations are performed to illustrate our theoretical results. Copyright © 2017 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

The seven members of the tumor necrosis factor receptor (TNF-R)-associated factor (TRAF) family of intracellular proteins were originally discovered and characterized as signaling adaptor molecules coupled to the cytoplasmic regions of receptors of the TNF-R superfamily. Functionally, TRAFs act both as a scaffold and/or enzymatic proteins to regulate activation of mitogen-activated protein kinases (MAPKs) and transcription factors of nuclear factor-κB family (NF-κB). Given the wide variety of stimuli intracellularly conveyed by TRAF proteins, they are physiologically involved in multiple biological processes, including embryonic development, tissue homeostasis, and regulation of innate and adaptive immune responses. In the last few years, it has become increasingly evident the involvement of TRAF7, the last member of the TRAF family to be discovered, in the genesis and progression of several human cancers, placing TRAF7 in the spotlight as a novel tumor suppressor protein. In this paper, we review and discuss the literature recently produced on this subject. J. Cell. Physiol. 232: 1233-1238, 2017. © 2016 The Authors. Journal of Cellular Physiology Published by Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

An infection-age virus dynamics model for human immunodeficiency virus (or hepatitis B virus) infections with saturation effects of infection rate and immune response is investigated in this paper. It is shown that the global dynamics of the model is completely determined by two critical values R0, the basic reproductive number for viral infection, and R1, the viral reproductive number at the immune-free infection steady state ( R1< R0). If R0<1, the uninfected steady state E0 is globally asymptotically stable; if R0>1 > R1, the immune-free infected steady state E∗ is globally asymptotically stable; while if R1>1, the antibody immune infected steady state [ABSTRACT FROM AUTHOR]

In this paper, we formulate a ( n + 3)-dimensional nonlinear virus dynamics model that considers n-stages of the infected cells and n + 1 distributed time delays. The model incorporates humoral immune response and general nonlinear forms for the incidence rate of infection, the generation and removal rates of the cells and viruses. Under a set of conditions on the general functions, the basic infection reproduction number [ABSTRACT FROM AUTHOR]

Background and Objectives Red blood cell alloimmunization is associated with haemolytic reactions and severe clinical consequences. The rate of alloimmunization in multitransfused patients such as thalassaemia is high that is a major challenge. The present meta-analysis study was conducted to determine the prevalence of alloimmunization in Iranian thalassaemia patients. Materials and Methods This study was conducted based on the computerized literature database. English and non-English articles were searched from 1994 to 2015. Alloimmunization rates and 95% CI calculated by random-effect model. Statistical analysis was performed using Stata 11.2, and Arc GIS 10.3 was used for map construction. Results Eighteen papers from 297 studies involving 4677 patients met our inclusion criteria. The prevalence of alloimmunization in Iranian thalassaemia was 10%( CI 95%: 7-13). The most prevalent alloantibody was anti-K (37%), followed by anti-D (29%) and anti-E (20%) in the country. Conclusion The prevalence of alloimmunization among Iranian thalassaemia has not been decreased from 1994 to 2013. In spite of detecting D antigen in pretransfusion test, the rate of anti-D is high in our population. It shows the importance of more investigation on data on D variants. Although the rate of alloimmunization is low in Iran comparing to many other countries, there is a need to adopt some strategies to reduce alloimmunization. [ABSTRACT FROM AUTHOR]

1. Immune priming refers to improved protection of the host after a second encounter with the same parasite or pathogen. This phenomenon is similar to that of adaptive immunity in vertebrates. 2. There is evidence to suggest that this improved protection can be species/strain-specific and can protect organisms for a lifetime. These two attributes, along with a biphasic immune response, are essential characteristics of immune priming and form the basis for the effectiveness of resistance to parasites and pathogens. 3. This paper considers the effect of immune priming within and across generations, the influence of a heterologous challenge during immune priming and the importance of testing the immune response with natural pathogens. 4. The analysis presented takes into account the multifaceted nature of the invertebrate immune response. The lack of evidence suggesting that the bacterial microbiome plays a complementary role in the immune priming outcome is discussed. 5. Finally, the cost of immune priming is explored. This is a poorly investigated issue, which could help to explain why there is a paucity of evidence in support of immune priming. [ABSTRACT FROM AUTHOR]

In this paper, we investigate the dynamical properties for a model of delay differential equations, which describes a virus-immune interaction in vivo. By analyzing corresponding characteristic equations, the local stability of the equilibria for infection-free, antibody-free, and antibody response and the existence of Hopf bifurcation with antibody response delay as a bifurcation parameter at the antibody-activated infection equilibrium are established, respectively. Global stability of the equilibria for infection-free, antibody-free, and antibody response, respectively, also are established by applying the Lyapunov functionals method. The numerical simulations are performed in order to illustrate the dynamical behavior of the model. Copyright © 2016 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Myeloid-derived suppressor cells (MDSC) are important to the tumour microenvironment as they actively suppress the immune system and promote tumour progression and metastasis. These cells block T-cell activation in the tumour microenvironment, preventing anti-tumour immune activity. The ability of a treatment to alter the suppressive function of these cells and promote an immune response is essential to enhancing overall therapeutic efficacy. Interleukin-12 (IL-12) has the potential not only to promote anti-tumour immune responses but also to block the activity of cells capable of immune suppression. This paper identifies a novel role for IL-12 as a modulator of MDSC activity, with implications for IL-12 as a therapeutic agent. Treatment with IL-12 was found to alter the suppressive function of MDSC by fundamentally altering the cells. Interleukin-12-treated MDSC exhibited up-regulation of surface markers indicative of mature cells as well as decreases in nitric oxide synthase and interferon-γ mRNA both in vitro and in vivo. Treatment with IL-12 was also found to have significant therapeutic benefit by decreasing the percentage of MDSC in the tumour microenvironment and increasing the percentage of active CD8 T cells. Treatment with IL-12 resulted in an increase in overall survival accompanied by a reduction in metastasis. The findings in this paper identify IL-12 as a modulator of immune suppression with significant potential as a therapeutic agent for metastatic breast cancer. [ABSTRACT FROM AUTHOR]

The article presents abstracts of several studies on hepatology. They include "Role of Hepatic Stellate Cells in Modulation of Immune Responses: A Mechanistic Insight into Hepatic Tolerance," "Three-Grade Criteria of Radical Resection for Primary Liver Cancer," "Meaning Making Among Survivors of Liver Cancer in Hong Kong," and "A Glycoproteome Database of Normal Human Liver Tissue."

Plaque-induced periodontal diseases occur in response to the accumulation of dental plaque. Disease manifestation and progression is determined by the nature of the immune response to the bacterial complexes in plaque. In general, predisposing factors for these periodontal diseases can be defined as those factors which retain or hinder the removal of plaque and, depending upon the nature of the immune response to this plaque, the disease will either remain stable and not progress or it may progress and result in chronic periodontitis. In contrast, modifying factors can be defined as those factors that alter the nature or course of the inflammatory lesion. These factors do not cause the disease but rather modify the chronic inflammatory response, which, in turn, is determined by the nature of the innate and adaptive immune responses and the local cytokine and inflammatory mediator networks. Chronic inflammation is characterized by vascular, cellular and repair responses within the tissues. This paper will focus on how common modifying factors, such as smoking, stress, hormonal changes, diabetes, metabolic syndrome and HIV/AIDS, influence each of these responses, together with treatment implications. As treatment planning in periodontics requires an understanding of the etiology and pathogenesis of the disease, it is important for all modifying factors to be taken into account. For some of these, such as smoking, stress and diabetic control, supportive health behavior advice within the dental setting should be an integral component for overall patient management. [ABSTRACT FROM AUTHOR]

In this paper, a class of virus infection model with Beddington-DeAngelis infection function and cytotoxic T-lymphocyte immune response is investigated. Time delay in the immune response term is incorporated into the model. We show that the dynamics of the model are determined by the basic reproduction number R1 and the immune response reproduction number R1 1. If R0 ≤, 1 then the infection-free equilibrium is globally asymptotically stable. If R1 > 1, then the immune-free equilibrium is globally asymptotically stable. If inline image, then the stability of the interior equilibrium is investigated. We conclude that Hopf bifurcation occurs as the time delay passes through a critical value. Numerical simulations are carried out to support our theoretical conclusion well. [ABSTRACT FROM AUTHOR]

The prevalence of apical periodontitis ( AP) in Europe has been reported to affect 61% of individuals and 14% of teeth, and increase with age. Likewise, the prevalence of root canal treatment ( RCT) in Europe is estimated to be around 30-50% of individuals and 2-9% of teeth with radiographic evidence of chronic persistent AP in 30-65% of root filled teeth ( RFT). AP is not only a local phenomenon and for some time the medical and dental scientific community have analysed the possible connection between apical periodontits and systemic health. Endodontic medicine has developed, with increasing numbers of reports describing the association between periapical inflammation and systemic diseases. The results of studies carried out both in animal models and humans are not conclusive, but suggest an association between endodontic variables, that is AP and RCT, and diabetes mellitus ( DM), tobacco smoking, coronary heart disease and other systemic diseases. Several studies have reported a higher prevalence of periapical lesions, delayed periapical repair, greater size of osteolityc lesions, greater likelihood of asymptomatic infections and poorer prognosis for RFT in diabetic patients. On the other hand, recent studies have found that a poorer periapical status correlates with higher HbA1c levels and poor glycaemic control in type 2 diabetic patients. However, there is no scientific evidence supporting a causal effect of periapical inflammation on diabetes metabolic control. The possible association between smoking habits and endodontic infection has also been investigated, with controversial results. The aim of this paper was to review the literature on the association between endodontic variables and systemic health (especially DM and smoking habits). [ABSTRACT FROM AUTHOR]

In this paper, a humoral and cellular immunity virus dynamics model with the Beddington-DeAngelis incidence rate is set up. We derive the basic reproductive number R0, the cytotoxic T lymphocytes immune response reproductive number R1, the humoral immune response reproductive number R2, humoral immune response competitive reproductive number R3, and cytotoxic T lymphocytes immune response competitive reproductive number R4, and a full description of the relation between the existence of the equilibria and reproductive numbers is given. The global properties of the five equilibria are obtained by constructing Lyapunov functions. Copyright © 2014 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Summary: Mass vaccination of the global population against SARS‐CoV‐2 will, we hope, turn the tide against this devastating pandemic. To complement vaccinations, better tools are needed to enable viral infections and immunological protection to be monitored. Accurate tools provide sound data for informed decision‐making at many levels, from personal to governmental. The measurement of viral RNA is currently routinely used to detect active infections, but only gives a positive result during infection and is unable to reveal historic infections. Tests involving a detection of SARS‐CoV‐2‐specific antibodies can reveal prior exposures to virus and can measure anti‐viral immune responses induced after natural infection or after vaccination. They may eventually also be used to predict an individual's likelihood of becoming re‐infected. Here, we report on the development of a sensitive ELISA technique to detect multiple isotypes of antibodies against the spike glycoprotein, in samples of both serum and saliva. This paper provides an important step towards understanding the immune response to SARS‐CoV‐2 and may therefore eventually help us to effectively control it. [ABSTRACT FROM AUTHOR]

In this paper, a mathematical model for HIV-1 infection with antibody, cytotoxic T-lymphocyte immune responses and Beddington-DeAngelis functional response is investigated. The stability of the infection-free and infected steady states is investigated. The basic reproduction number R0 is identified for the proposed system. If R0 < 1, then there is an infection-free steady state, which is locally asymptotically stable. Further, the infected steady state is locally asymptotically stable for R0 > 1 in the absence of immune response delay. We use Nyquist criterion to estimate the length of the delay for which stability continues to hold. Also the existence of the Hopf bifurcation is investigated by using immune response delay as a bifurcation parameter. Numerical simulations are presented to justify the analytical results. Copyright © 2014 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

In this paper, the global stability of a virus dynamics model with intracellular delay, Crowley-Martin functional response of the infection rate, and CTL immune response is studied. By constructing suitable Lyapunov functions and using LaSalles invariance principle, the global dynamics is established; it is proved that if the basic reproductive number, R0, is less than or equal to one, the infection-free equilibrium is globally asymptotically stable; if R0 is more than one, and if immune response reproductive number, R0, is less than one, the immune-free equilibrium is globally asymptotically stable, and if R0 is more than one, the endemic equilibrium is globally asymptotically stable. Copyright © 2014 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Systemic immune response via the Immune deficiency pathway requires Drosophila inhibitor of apoptosis protein 2 to activate the NF-κB transcription factor Relish. Malpighian tubules (MTs), simple epithelial tissue, are the primary excretory organs, performing additional role in providing protection to Drosophila against pathogenic infections. MTs hold a strategic position in Drosophila as one of the larval tissues that are carried over to adults, unlike other larval tissues that are histolysed during pupation. In this paper we show that Diap2 is an important regulator of local epithelial immune response in MTs and depletion of Diap2 from MTs, increases susceptibility of flies to infection. In the absence of Diap2, activation and translocation of Relish to the nucleus is abolished and as a consequence the production of IMD pathway dependent AMPs are reduced. Ion channels, (Na+/K+)-ATPase and V-ATPase, are important for the immune response of MTs and expression of AMPs and the IMD pathway genes are impaired on inhibition of transporters, and they restrict the translocation of Relish into the nucleus. We show that Diap2 could be regulating ion channels, as loss of Diap2 consequently reduces the expression of ion channels and affects the balance of ion concentrations which results in reduced uric acid deposition. Thus Diap2 seems to be a key regulator of epithelial immune response in MTs, perhaps by modulating ion channels. J. Cell. Physiol. 229: 1078-1095, 2014. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]