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Lyme disease triggered by infected ticks can affect over 300,000 people/year in USA and 65,000 people/year in Europe mainly in spring and summer. The early symptoms fever, headache and tiredness can evolve if left untreated in joint pains, facial paralysis, headaches with neck stiffness, heart palpitations. Moreover about 10 - 20% of patients will continue to develop months/years to come joint pains, memory issues and tiredness. Humans from all the continents interact with ticks and this interaction is measured indirectly, by relating tick population abundance, pathogen prevalence, and registered human borreliosis. Lyme borreliosis caused by bacteria of the Borrelia burgdorferi sensu lato species, is the most widespread tick-borne infection registered in the northern hemisphere. Diagnostics starts with the clinical evaluation of the infected patient and is complemented by laboratory testing. FDA recommendation published in 2019 recommend a two-test methodology, as a first test the methodology is based on sensitive enzyme immunoassay (EIA) (replaceable with an immunofluorescence assay), followed by a western immunoblot (WB) assay for positive or equivocal results. These tests have several down -falls thus focusing on using various proteomic/metabolomic/genomic technologies for early stages of infection identification these down-falls can be surpassed. Borrelia burgdorferi has several proteins that can be involved in the hosts immune response. Identification of protective epitopes that could be used to develop a new vaccine becomes imperative as new prophylactic methods can reduce the incidence of this wide-spread disease. [ABSTRACT FROM AUTHOR]

Among skin pathologies, psoriasis is one of the most challenging disorders in terms of therapy and clinical monitoring of the patient.Psoriasis is a chronic inflammatory skin condition that has an autoimmune mechanism mediated by T cells, with involvement of innate immune cells.An important role is played by different subsets ofT-helper lymphocytes, as well as a number of proinflammatory cytokines that maintain the chronic inflammatory state. Although some evidence suggests that NK cells play animportant role in psoriasis, their contribution to disease's development and progression remains incompletely understood. Experimental models are an indispensable tool in psoriasis research for both pathogenesis evaluation and for possible therapeutic targets identification. Due to its advantages, experimental models such as the Imiquimod-based mice model is one of the most popular animalmodel to study psoriasiform dermatitis in mice. In order to highlight the role of NK cells in the development of psoriasis, we performed the Imiquimod-based mice model and analysed NK cells distribution and phenotype by flow cytometry. Skin inflammation induced by Imiquimodwas assessed based on in vivo parameters (erythema, desquamation, thickening), PASI score, evaluation of splenomegaly and pathological examination. NK cells distribution was evaluated on three immune levels: peripheral blood spleen and skin There were quantified NK cells subsets based on the expression of CD27 and CDUb, and NK1.1+CD11c+CD45R+subset. The expression of CD43, KLRG1 and CD69, markers with an important role in NK cells maturation and activation, was analysed.Our data show that, although a somewhat neglected cell in psoriasis, NKs correlate with the gravity of the auto-immune disease. [ABSTRACT FROM AUTHOR]

Psoriasis (Ps) is a chronic inflammatory immune-mediated disease with skin and joint manifestations, characterized by abnormal and rapid proliferation of keratinocytes and infiltration of psoriatic lesions with immune cells. Extensive literature suggests that Ps is a T-cell mediated disease its pathogenesis being highly related to innate and adaptative immune cells. Although natural killer (NK) cells are involved in the inflammatory process of Ps through pro-inflammatory cytokine secretion (tumor necrosis factor α, interferon γ), their role in this pathology is not yet fully elucidated. In order to study the involvement of NK subpopulations in the pathogenesis of Ps we used the imiquimod-based mouse model of psoriasiform dermatitis and NK cells complex phenotype patterns from peripheral blood (PB) and spleen were investigated. Skin inflammation and the disease severity were assessed using in vivo measurements (erythema, desquamation and induration parameters, PASI modified score), splenomegaly assessment and histopathological evaluation. Phenotypic characterization of NK cells in imiquimod (IMQ)-treated mice was performed by flow cytometry, for both PB and spleen cell suspension. A large panel of surface markers was used: maturation and activation markers [cluster of differentiation (CD)49b, CD11b, CD43, CD27, KLRG1, CD335, CD69, CD28, gp49R, CD45R, CD11c] and markers for cytokine receptors (CD25, CD122, CD132). Our experimental data showed important differences in IMQ-treated mouse NK cell phenotype as compared to control group. The maturation markers (CD11b, CD43, CD27, KLRG1) were found increased on NK cells, in periphery and spleen, while CD49b+NK1.1+ was significantly lower, and the alterations correlated with the severity of the disease. Our findings reflect the immune engagement toward activatory profile of NK cells and draw attention to evaluating Ps intensity correlated with the mature profile of circulating NK cells. [ABSTRACT FROM AUTHOR]

The immune system of a child has a degree of immaturity that is maintained until 6–7 years of age. Immaturity may be due to age-related functional disorders in the immune response. A healthy child can contract a series of infections which contribute to the maturation of the immune system during the pre-pubertal period. If repeated infections with prolonged or severe complications occur during childhood, the presence of an immunodeficiency should then be considered. Much more frequent than primary immunodeficiency are recurrent infections (frequently involving the upper respiratory tract), which are less severe and occur under the conditions of an immune system with no apparent major defects. A child can present with 4 to 8 episodes of respiratory infections within a year, during the first 5 years of its life. The average duration of infection is 8 days and up to 2 weeks; if the child presents with 3 episodes of acute infections over a period of 6 months, the respiratory infections are then considered recurrent. The aim of this study was to identify the immunological changes or deviations that cause this clinical syndrome in children. For this purpose, 30 children with recurrent respiratory infections and 10 healthy children were included. Immunoglobulin levels were examined and immunophenotyping was performed. We found that the serum immunoglobulin levels were in the normal range in 70% of the children. On the contrary, our data revealed changes in peripheral cell populations, the most important being the decrease in the T-cluster of differentiation (CD)8+ and total B cell percentages and the increase in the number of memory B cells. The data obtained herein indicated that the decrease in the number of total B cells was mainly due to the decrease in the number of naive IgD+ B cells. On the whole, the findings of this study indicate that recurrent respiratory infections may be associated with an altered cellular immune response. In such situations, the investigation of immunological parameters, such as T and B cell subtypes could complete the clinical diagnosis and guide the treatment strategy, thus increasing the quality of life of patients. [ABSTRACT FROM AUTHOR]

Melanoma is responsible for most skin cancer deaths in humans. The immune system plays a major role in regulating tumor cell proliferation by initiating defence responses against tumor aggression. Research on murine cancer models allow for a better understanding of immune response in malignancies, revealing specific changes of the immune status in the presence of tumors. Melanoma resistance to conventional therapies and its high immunogenicity justify the development of new therapies. These features reinforce melanoma as a suitable model for studying antitumor immunity. Recent findings on NK cell activation in cancer patients indicate that several important parameters, such as tumor capacity to modulate the function and phenotype of NK cells, require consideration for the choice of an NK-based therapy. In this study, we investigated T-CD4+ and T-CD8+ lymphocytes, B lymphocytes and NK cells in peripheral blood and spleen cells suspension from melanoma-bearing mice compared to healthy controls in order to assess the potential for tumor growth-promoting immunosuppression. Our results indicate that in a melanoma-bearing mouse model the percentage of NK cells in spleen is reduced and that their phenotype is different compared to control mouse NK cells. [ABSTRACT FROM AUTHOR]

Psoriasis is a T cell mediated, chronic inflammatory autoimmune skin disease that affects up to 2–3% of the global population and leads to a decrease in quality of life. Experimental data accumulated in recent years highlighted the important role played by the immune system in the pathogenesis of this disease. Non-human psoriasis models are an important research tool that attempts to reproduce the clinical features of the disease in order to explain the pathogenesis of psoriasis and to identify possible therapeutic targets. Imiquimod-based murine model of psoriatic dermatitis is an alternative to traditional models of experimental psoriasis in mice and the induced dermatitis closely mimics the pathologic changes in human psoriasis. In order to emphasize changes in immune cell populations involved in lesion pathogenesis, we performed a murine model of psoriasiform dermatitis model by topical IMQ application. The progress and the severity of IMQ-induced skin inflammation were clinically (PASI score) and histopathologically evaluated. The immunological changes induced by IMQ treatment in lymphocyte populations from peripheral blood and spleen were evaluated by flow cytometry. The main changes observed in peripheral blood were the significantly increased T-CD8a+ lymphocyte and NK1.1+ cell percentages and the decreased T-CD4+ and B lymphocyte percentages in IMQ-treated mice. In spleen samples, lymphocytes showed the same tendency of variation as in peripheral blood, but without statistical significance. A significant decrease of B cells percentages was observed in spleen suspensions. Data obtained in skin samples may suggest the involvement of CD3ε+, CD4+ and CD8a+ cells in the lesional process. This murine model was analyzed by performing a basic cellular profile at three levels: peripheral blood, spleen and skin. The evaluation aimed to establish the immune framework of this experimental model that could further be used for etipathogenic mechanism identification and/or for studies regarding targeted therapies. [ABSTRACT FROM AUTHOR]

The immune system is dysfunctional in cancer, and therapeutic approaches designated to restore immunity and increase long-term overall survival are desirable. The role of immunotherapy is to trigger the immune system to recognize and destroy tumor cells. Interleukin-15 (IL-15) is a member of the common gamma-chain (γc) cytokines that promote the differentiation and expansion of T cells, B cells and natural killer (NK) cells, leading to enhanced antitumor responses. This suggests that IL-15 is a promising candidate for anticancer therapy. Renewed interest in cancer immunotherapy has led to an increased number of preclinical studies and clinical trials that have investigated the reliability and potency of IL-15-based agents, not only as single therapy, but also in combination with others. This review provides a description of these studies which show the advantages and disadvantages of IL-15 as an immunotherapeutic agent. We present here the role of IL-15 and pharmacologically improved IL-15 superagonists as a single treatment or in combination with other therapeutic agents. [ABSTRACT FROM AUTHOR]

We assessed Helper T-cell involvement and possibilities to quantify the cell-based immune response in systemic autoimmune diseases (SAID) in 14 systemic lupus erythematosus (SLE) and 7 rheumatoid arthritis (RA) patients. The goals of investigation were T-CD4+/T-CD8+ ratio, regulatory T cells (Treg) status and TH1/TH2 serum cytokine profiles (IFN-gamma and IL-2, respectively IL-4 and IL-6). SLE group proved significant decreased average Treg value as compared to RA group and controls and showed significant low Treg incidence (86% patients). The distribution of high T-CD4+/T-CD8+ ratio registered no significant distinction among LES and RA groups. SAID patients presented low serum IFN-gamma (86% RA, 60% SLE), high IL-2 (57% RA) and high IL-6 (53% LES), but no significant IL-4 modification. We conclude that Treg percentage remains the only cellular criterion for SAID immune evaluation. In the same time, different secretion mechanisms seem to be involved in SAID, i.e. TH2 in SLE and TH1 in RA.