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The first encounter of mucosal barriers with the microbiota initiates host-microbiota feedback loops instructing the tailored development of both the immune system and microbiota at each mucosal site. Once established, balanced immunological interactions enable symbiotic relationships with the microbiota in adult life. This process has been extensively investigated in the mammalian monolayer epithelium-covered intestine and lung mucosae; however, the postnatal mechanisms engaged by the oral mucosa to establish homeostasis are currently being discovered. Here, we discuss the early life dialogue between the oral mucosa and the microbiota, with particular emphasis on the central role the multilayer epithelium plays to protect the oral mucosa. These intricate and unique postnatal immunological processes shape oral homeostasis, which can potentially affect buccal and systemic health in adult life.

Pain is among the most widespread chronic health condition confronting society today and our inability to manage chronic pain contributes to the opioid abuse epidemic in America. The immune system is known to contribute to acute and chronic pain, but only limited therapeutic treatments such as non-steroid anti-inflammatory drugs have resulted from this knowledge. The last decade has shed light on neuro-immune interactions mediating the development, maintenance, and resolution of chronic pain. Here, we do not aim to perform a comprehensive review of all immune mechanisms involved in chronic pain, but to briefly review the contribution of the main cytokines and immune cells (macrophages, microglia, mast cells and T cells) to chronic pain. Given the urgent need to address the Pain crisis, we provocatively propose to repurpose/reposition FDA-approved immunomodulatory drugs for their potential to alleviate chronic pain. Repositioning or repurposing offers an attractive way to accelerate the arrival of new analgesics.

Objective This review provides an overview of our current understanding of the mechanisms of food protein–induced enterocolitis syndrome (FPIES). Data Sources To capture recent articles published since our previous comprehensive review on the pathophysiology of FPIES, we performed a literature search through PubMed database, using the search terms FPIES and food protein–induced enterocolitis syndrome from 2016 to the current year. Study Selections Studies in English containing biomarker or immune data were reviewed and summarized. Results Studies of peripheral blood fail to exhibit evidence of antigen-specific humoral or cellular immunity underlying clinical reactivity to foods in FPIES. However, growing evidence suggests a robust systemic innate immune activation occurring during FPIES reactions and the activation of neuroendocrine pathways. Conclusion FPIES reactions are associated with marked activation of innate immune and neuroendocrine pathways; however, the mechanism underlying the specific recognition of foods remains elusive.

This experimental studies investigated the protective efficiencies and the potential immune mechanisms of vibrio monovalent and polyvalent autogenous formalin-inactivated whole-cell bacterins (FKC) in Gilthead sea bream (Sparus aurata) cultured in Egypt. Two months post-vaccination, the relative percentage survival (RPS) was estimated after challenge with the vaccine's homologues pathogenic strains. The survival values were 100% and 83.3% in groups immunized with monovalent V. alginolyticus or V. parahaemolyticus FKC bacterins, respectively. On the other hand, survival values were 91.75% and 75% in fish groups subjected to polyvalent (V. parahaemolyticus O11: K40V. alginolyticus) and (V. parahaemolyticus O3: K6V. alginolyticus) FKC bacterins, respectively. Overall, the tested vaccine preparations were significantly increased (P 0.05) the agglutination antibody titer, phagocytic activity, respiratory burst activity, when compared to the non-immunized control group. The current results conclude that, autogenous Vibrio vaccines provoked a promising protection against vibriosis in Gilthead sea bream cultured in Egypt, it was superior in monovalent FKC V. alginolyticus vaccine and polyvalent FKC of V. parahaemolyticus O11: K40 with V. alginolyticus vaccine that could be useful means of prevention and control of vibriosis.

The hydrotherapy centre in Avene, France, is used extensively to treat inflammatory skin diseases. Nevertheless, the immune mechanisms targeted by Avene Thermal Spring Water (TSW) are not fully understood. Here, we review the main results reported regarding the effects of Avene TSW on the immune system. In particular, mast cells, dendritic cells (DCs) and CD4+ T cells have been shown to be modulated by Avene TSW. All in all, the studies carried out on the effects of Avene TSW on leucocytes indicate that this water is endowed with a tolerogenic potential.

Despite significant research efforts, only a few treatment approaches have been developed for hepatocellular carcinoma (HCC). In recent years, immune checkpoint inhibitors (anti-PD-1, anti-PD-L1, and anti-CTLA-4 antibodies) have exhibited potential therapeutic effects for advanced HCC. With the development of gene-editing technologies, gene-sequencing technologies, big data strategies, and artificial intelligence algorithms, engineered immune cell infusion and personalized cancer vaccine therapy have emerged as important directions for anti-HCC treatment. Combining different immunotherapies or combining immunotherapies with conventional therapeutic approaches may provide synergistic effects and facilitate the development of personalized medicine. In this study, we provide an overview of the liver immunoanatomy, the potential immune mechanisms of HCC, and current (pre)clinical developments in this field.

Cancer metastasis is the leading cause of cancer-related death. Circulating tumor cells (CTCs) are shed into the bloodstream from either primary or metastatic tumors during an intermediate stage of metastasis. In recent years, immunotherapy has also become an important focus of cancer research. Thus, to study the relationship between CTCs and immunotherapy is extremely necessary and valuable to improve the treatment of cancer. In this review, based on the advancements of CTC isolation technologies, we mainly discuss the clinical applications of CTCs in cancer immunotherapy and the related immune mechanisms of CTC formation. In order to fully understand CTC formation, sufficiently and completely understood molecular mechanism based on the different immune cells is critical. This understanding is a promising avenue for the development of effective immunotherapeutic strategies targeting CTCs.

The pulmonary immune system plays a vital role in protecting the delicate structures of gaseous exchange against invasion from bacterial pathogens. With antimicrobial resistance becoming an increasing concern, finding novel strategies to develop vaccines against bacterial lung diseases remains a top priority. In order to do so, a continued expansion of our understanding of the pulmonary immune response is warranted. While some aspects are well characterized, emerging paradigms such as the importance of innate cells and inducible immune structures in mediating protection provide avenues of potential to rethink our approach to vaccine development. In this review, we aim to provide a broad overview of both the innate and adaptive immune mechanisms in place to protect the pulmonary tissue from invading bacterial organisms. We use specific examples from several infection models and human studies to depict the varying functions of the pulmonary immune system that may be manipulated in future vaccine development. Particular emphasis has been placed on emerging themes that are less reviewed and underappreciated in vaccine development studies.

In the part I of a literature review of modern national and foreign publications dedicated to the problem of immune disorders in acute pyelonephritis, information on the role of innate and adaptive immunity in the pathogenesis of acute pyelonephritis is summarized and systematized. The relationship between the pathogens and immune system, in particular the ability of pathogens to overcome the protective immune mechanisms are discussed. The role of neutrophilic granulocytes as well as cellular immunity in the pathogenesis of acute pyelonephritis is shown. The changes in level of pro- and anti-inflammatory cytokines are separately highlighted. In conclusion, perspective directions for the studies in the area of immune disorders in acute pyelonephritis are proposed.

The biological milieu and clinical picture of myelodysplastic syndromes (MDS) is characterised by a variety of immune mechanisms and manifestations, including an increased frequency of autoimmune disorders. The present review will try to shed some light on the potential clinical and pathogenetic implications of these immune processes in MDS by focusing on the beneficial effects exerted by some MDS-modifying therapies on autoimmune manifestations.

Summary Context: with the arrival of immunotherapy in cancer care, it is no longer the drug that will destroy the tumour, but the patient himself, thanks to his immune system. We do, however, encounter two important problems. Why do only 20 to 30% of patients respond to this treatment? Why do some patients switch to autoimmunity. Method: by studying the exact immune mechanisms involved in immunotherapy, we sought, respecting the principle of similarity, homeopathic medicines able to support and modulate the immune responses induced by immunotherapy. Results: of course, Silicea is the traditional and reliable immune modulator, but there is also a new interesting medicine which belongs to the Lanthanides group: Dysprosium metallicum. In medium dilution they appear to be the two best medicine-candidates. The constitutional remedy of the patient, when it is known, can also be considered in this situation. Clinically, we obtained good preliminary results on the immune response and less autoimmune side effects compared to the figures expected in scientific literature. Conclusion: the challenge of a good response and a good tolerance to immunotherapy is real. This should prompt us to propose innovative homeopathic support protocols, such as Silicea and Dysprosium metallicum, which can encourage the mechanisms of action of immunotherapy, while preventing side effects. Clinical studies are now needed to evaluate our work.

Enterococcus faecalis, a ubiquitous member of the healthy human gut microbiota, is also a common opportunistic pathogen and leading cause of nosocomial infections. This tenacious microbe is well adapted to infect and persist in multiple niches within the mammalian host and can rapidly tune its metabolism to respond to new environments, enabling infection in sites including the gastrointestinal tract, urinary tract, wounded epithelium, heart, and blood. In order to withstand and persist in the face of host immune responses, E. faecalis has an arsenal of strategies to suppress, evade, or inactivate innate and adaptive immune mechanisms. In this review, we present the variety of ways E. faecalis modulates the immune response, enabling this otherwise innocuous gut commensal to transition and persist as a pathogen.

Thrombocytes in vertebrates other than mammals, inter alia in fish, are analogues of platelets in mammals. In Osteichthyes, these cells take part in haemostatic processes, including aggregation and release reactions in cases of blood vessel damage, and in the immune response development as well. This paper discusses the development of thrombocytes in Osteichthyes, taking into account the need to make changes to the concept of grouping progenitor cells as suggested in the literature. The following pages present the morphological and cytochemical properties of thrombocytes as well as their defence functions, and also point out differences between thrombocytes in fish and platelets in mammals. The paper further highlights the level of thrombocytes’ immune activity observed in fish and based on an increased proportion of these cells in response to antigenic stimulation, on morphological shifts towards forms characteristic of dendritic cells after antigenic stimulation and on the presence of surface structures and cytokines released through, inter alia, gene expression of TLR receptors, MHC class II protein-coding genes and pro-inflammatory cytokines. The study also points out the need to recognise thrombocytes in Osteichthyes as specialised immune cells conditioning non-specific immune mechanisms and playing an important role in affecting adaptive immune mechanisms.

The skin interfaces with the external environment and is home to a myriad of immune cells that patrol the barrier to ward off harmful agents and aid in tissue repair. The formation of the cutaneous immune arsenal begins before birth and evolves throughout our lifetime, incorporating exogenous cues from microbes and inflammatory encounters, to achieve optimal fitness and function. Here, we discuss the context-specific signals that drive productive immune responses in the skin epithelium, highlighting key modulators of these reactions, including hair follicles, neurons, and commensal microbes. We thus also discuss the causal and mechanistic underpinning of inflammatory skin diseases that have been revealed in recent years. Finally, we discuss the non-canonical functions of cutaneous immune cells including their burgeoning role in epithelial regeneration and repair. The rapidly growing field of cutaneous immunity is revealing immune mechanisms and functions that can be harnessed to boost skin health and treat disease.

Higher organisms are all born with general immunity as well as with, increasingly, more specific immune systems. All immune mechanisms function with the intent of aiding the body in defense against infection. Internal and external factors alike have varying effects on the immune system, and the immune response is tailored specifically to each one. Accompanying the components of the human innate and adaptive immune systems are the other intermingling systems of the human body. Increasing understanding of the body’s immune interactions with other systems has opened new avenues of study, including that of the microbiome. The microbiome has become a highly active area of research over the last 10 to 20 years since the NIH began funding the Human Microbiome Project (HMP), which was established in 2007. Several publications have focused on the characterization, functions, and complex interplay of the microbiome as it relates to the rest of the body. A dysfunction between the microbiome and the host has been linked to various diseases including cancers, metabolic deficiencies, autoimmune disorders, and infectious diseases. Further understanding of the microbiome and its interaction with the host in relation to diseases is needed in order to understand the implications of microbiome dysfunction and the possible use of microbiota in the prevention of disease. In this review, we have summarized information on the immune system, the microbiome, the microbiome’s interplay with other systems, and the association of the immune system and the microbiome in diseases such as diabetes and colorectal cancer.

Objective With the increasing prevalence of celiac disease (CD) in the population, possible risk factors are under investigation. Environmental and genetic factors that trigger the immune response have been analyzed for many years. This study investigates the presence of CD in children with rotavirus infection. Rotavirus infection is thought to be a risk factor for CD. Methods Included in the study were 105 of 160 pediatric patients hospitalized due to symptomatic rotavirus infection between 2012 and 2018. These children were screened for CD 45.6 ± 18.2 (14–90) months following the rotavirus infection diagnosed with CD as per ESPGHAN guidelines. Results A total of 105 pediatric patients who had rotavirus gastroenteritis were included in the study. The age of the children with rotavirus infection was 3.98 ± 1 (2–6) months. In terms of CD, it was 45.6 ± 18.2 months. Around 14 to 90 months later, patients were called for control. CD developed in four (3.8%) of the children with rotavirus, whereas none of the children in the control group developed CD. Conclusion Rotavirus infection may be a risk factor for CD through immune mechanisms. There are genetic and various environmental factors for the development of CD. Although the CD's occurrence on children who had rotavirus gastroenteritis in our study also supported this situation, there was no statistically significant difference.

The intestinal barrier is a selective system protecting the intestine against infections, consisting of many highly specialized immune mechanisms. These include physical and chemical mechanisms related to the secretion of mucus by goblet cells and the specific tight junction architecture of the intestinal epithelium. The most extensive intestinal protection system consists of the biological barrier associated with the collection of immune cells organized into Peyer’s patches. All these mechanisms undergo strong modification and maturation during the course of an individual’s life. By gradually closing and sealing the barrier, these intestinal mechanisms prepare the animal for all changes in the type of consumed food, which constitutes one of the most important evolutionary adaptation mechanisms.

In which we move from the small intestine and the immune mechanisms involved with its relationship to food and encounter the inflammatory bowel diseases affecting the other end of the gastrointestinal tract and its association with commensal bacteria. Once again, we come across the ‘great schism’ in the sidewall of the gastro archeological trench that divides the antibody-type from the cell-killing type of immune response with the conditions known as ulcerative colitis and Crohn’s disease lying on respective sides. We identify common pathways of these two conditions in the upper strata of the dig relating to the ‘on’ and ‘off’ switches of the adaptive immune system and we see how these are in turn controlled by deeper and older mechanisms. At the very bottom of our trench we reveal how ulcerative colitis and Crohn’s disease differ, by respectively dealing with invasion of microbes across the epithelial containment barrier, and the cellular containment barrier. Ultimately we dig down to the molecular switch that separates the two sides of the great schism and encounter some ancient secrets of life through association with a surprising location.

The human microbiota forms a life-long reciprocal relationship with the host influencing the innate and adaptive immune system. The pathogenesis of systemic lupus erythematosus (SLE) involves dysregulation of innate and adaptive immune mechanisms that normally function to defend against microbes, but instead turn against self-antigens. Loss of self-tolerance is one of the fundamental mechanisms of autoimmunity and the influence of the microbiota on this process is increasingly recognized. Loss of beneficial microbes or outgrowth of certain pathobionts driving innate or adaptive immune responses have recently been discovered in rheumatic diseases and will be reviewed in this chapter with a focus on SLE.

There is emerging evidence that resident microbiota communities, that is, the microbiota, play a key role in cancer outcomes and anticancer responses. Although this has been relatively well studied in colorectal cancer and melanoma, other cancers, such as breast cancer (BrCa), have been largely overlooked to date. Importantly, many of the environmental factors associated with BrCa incidence and progression are also known to impact the microbiota, for example, diet and antibiotics. Here, we explore BrCa risk factors from large epidemiology studies and microbiota associations, and more recent studies that have directly profiled BrCa patients' gut microbiotas. We also discuss how in vivo studies have begun to unravel the immune mechanisms whereby the microbiota may influence BrCa responses, and finally we examine how diet and specific nutrients are also linked to BrCa outcomes. We also consider future research avenues and important considerations with respect to study design and implementation, and we highlight some of the important unresolved questions, which currently limit our overall understanding of the mechanisms underpinning microbiota‐BrCa responses.

The ability to read, write, and edit genomic information in living organisms can have a profound impact on research, health, economic, and environmental issues. The CRISPR/Cas system, recently discovered as an adaptive immune system in prokaryotes, has revolutionized the ease and throughput of genome editing in mammalian cells and has proved itself indispensable to the engineering of immune cells and identification of novel immune mechanisms. In this review, we summarize the CRISPR/ Cas9 system and the history of its discovery and optimization. We then focus on engineering T cells and other types of immune cells, with emphasis on therapeutic applications. Last, we describe the different modifications of Cas9 and their recent applications in the genome-wide screening of immune cells. [BMB Reports 2021; 54(1): 59-69].

Children with chronic mucocutaneous candidiasis (CMC) experience recurrent infections with Candida spp. Moreover, immune dysregulation in the early life of these patients induces various autoimmune diseases and affects normal growth and development. The adaptive and innate immune system components play a significant role in anti-fungal response. This response is mediated through IL-17 production by T helper cells. Inborn errors in IL-17-mediated pathways or Candida spp. sensing molecules are known to cause CMC. In this review, we describe underlying immune mechanisms of monogenic primary immune deficiency disorders known to cause CMC. We will explore insights into current management of these patients and novel available therapies.

HBsAg seroclearance occurs rarely in the natural history of chronic hepatitis B (CHB) infection and is associated with improved clinical outcomes. Many factors are associated with HBsAg seroconversion, including immune and viral factors. However, the immune mechanisms associated with HBsAg seroclearance are still difficult to elucidate. HBsAg seroclearance is the ideal aim of HBV treatment. Unfortunately, this goal is rarely achieved with current treatments. Understanding the mechanisms of HBsAg loss appears to be important for the development of curative HBV treatments. While studies from animal models give insights into the potential immune mechanisms and interactions occurring between the immune system and HBsAg, they do not recapitulate all features of CHB in humans and are subject to variability due to their complexity. In this article, we review recent studies on these immune factors, focusing on their influence on CHB progression and HBsAg seroconversion. These data provide new insights for the development of therapeutic approaches to partially restore the anti-HBV immune response. Targeting HBsAg will ideally relieve the immunosuppressive effects on the immune system and help to restore anti-HBV immune responses.

This chapter considers the evidence for cancer-specific benefits and risks of physical activity and exercise. In spite of the considerable work on natural immune mechanisms against cancer, and the increasing attention to natural immune changes with exercise, the hypothesis that physical activity influences the incidence of and mortality from certain cancers consequent to the enhancement of natural immunity has not been systematically evaluated. Animal studies have focused on the exercise component of physical activity in relation to colon cancer. The chapter provides a framework for the later consideration of exercise-induced changes in natural immunity and how these may relate to cancer processes. Alternatively, exercise-induced changes in blood flow might result in greater delivery of natural killer cells, cytokines, and so on to tissue sites where tumors are proliferating; at this level, exercise would interact with the immune system to enhance cancer surveillance and decrease early tumor growth.

Humans with salt-sensitive (SS) hypertension demonstrate increased morbidity, increased mortality, and renal end-organ damage when compared with normotensive subjects or those with salt-resistant hypertension. Increasing evidence indicates that immune mechanisms play an important role in the full development of SS hypertension and associated renal damage. Recent experimental advances and studies in animal models have permitted a greater understanding of the mechanisms of activation and action of immunity in this disease process. Evidence favors a role of both innate and adaptive immune mechanisms that are triggered by initial, immune-independent alterations in blood pressure, sympathetic activity, or tissue damage. Activation of immunity, which can be enhanced by a high-salt intake or by alterations in other components of the diet, leads to the release of cytokines, free radicals, or other factors that amplify renal damage and hypertension and mediate malignant disease.

Host defenses against infection by viruses, bacteria, fungi, and parasites are critical to survival. It has been estimated that upwards of 7% of the coding genes of mammals function in immunity and inflammation. This high level of genomic investment in defense has resulted in an immune system characterized by extraordinary complexity and many levels of redundancy. Because so many genes are involved with immunity, there are many opportunities for mutations to arise that have negative effects. However, redundancy in the mammalian defense system and the adaptive nature of key immune mechanisms buffer the untoward outcomes of many such deleterious mutations.

The lung is a central organ for immune-environmental interactions ranging from tolerance against harmless substances to protection against pathogens, which are particularly sensitive to regulation by the intestinal microbiota. Airborne fungi, can cause variety of diseases, including allergies and inflammatory disorders, as well as life-threatening invasive infections. Remarkable differences exist between ubiquitous fungal species with regard to protective immune mechanisms. Recent data have surprisingly identified Aspergillus-specific regulatory T cells as an essential tolerance checkpoint and provided mechanistic insight for the loss of tolerance in the course of immune pathologies. Furthermore, pathogenic Th17 cells in Aspergillus-associated inflammatory disease seem to be induced by cross-reactivity to the intestinal commensal Candida albicans. Here we review and discuss what is known about fungus-specific T cell responses in the lung how they are modulated by the gut-lung axis and in particular discussing the modulation of adaptive immune responses by cross-reactivity to the microbiota.

Idiopathic inflammatory myopathies (IIMs) are chronic autoimmune disorders involving multiple organs, such as the muscle, skin, lungs and joints. Although the detailed pathogenesis of IIMs remains unclear, immune mechanisms have long been recognised as of key importance. Immune cells contribute to many inflammatory processes via intercellular interactions and secretion of inflammatory factors, and many studies have demonstrated the participation of a variety of immune cells, such as T cells and B cells, in the development of IIMs. Here, we summarise the current knowledge regarding immune cells in IIM patients and discuss their potential roles in IIM pathogenesis.

The immune system defends the body from various pathogens. Occasionally immune mechanisms fail in responding to antigens or they respond to self-antigens leading to severe complications like hypersensitivity, autoimmune disorders, cancer and AIDS. These conditions necessitate the use of compounds capable of modifying the immune system called immunomodulators. A large number of synthetic compounds are currently used for augmenting the immune system causing variety of side effects. Using natural biomolecules which are benign and economical can lead to safe immunomodulation. Application of plant metabolites for activating or suppressing the immune system is currently a fascinating area of research. This rational approach of immunomodulation has led to the discovery of many phytocompounds from known medicinal plants. Berberine, leonurine, piperine, gelselegine, chelerythrine and pseudo coptisine are some immunomodulatory agents derived from plants. Exploring plants with the use of innovative techniques will increase the choice of immunomodulators.

Literally, reproductive immunology was born in bovine on-farm reproduction where seminal experiments intended for developing methods for embryo transfer in cattle were performed. Actually, these experiments led to two of major concepts and fundamental principles of reproductive immunology using the bovine species as a model for biomedical research, namely the concept of acquired immunological tolerance and the paradox of the semiallogeneic bovine foetus whereby such organism can develop within an immunologically competent host. Peter Medawar, a scientist who together with Frank Macfarlande Burnet shared the 1960 Nobel Prize in physiology or medicine for discovery of acquired immunological tolerance, while studying dizygotic cattle twins, thereby giving birth to reproductive immunology. Also, these findings significantly influenced development of organ transplants and showed that using farm animals as models for studying transplantation immunology had general relevance for mammalian biology and health including those of humans. However, the interest for further research of the fascinating maternal immune influences on pregnancy and perinatal outcomes and of the prevention and treatment of immunologically mediated reproductive disorders in viviparous mammals of veterinary relevance by veterinary immunologists and reproductive clinicians have been very scarce regarding the application of nonspecific immunomodulatory agents for prevention and treatment of subfertility and infertility in pigs and cattle, but still broadening knowledge in this area and hold great potential for improving such therapy in the future. The aim of the current overview is to provide up-to-date information and explaining/translating relevant immunology phenomena into veterinary practice for specialists and scientists/clinicians in reproduction of animals. Link to the corrected article: [https://vet-erinar.vet.bg.ac.rs/handle/123456789/2052]

Treatment of medical device-related infections is challenging and recurrence is common. The main reason for this is that microorganisms adhere to the surfaces of medical devices and enter into a biofilm state in which they display distinct growth rates, structural features, and protection from antimicrobial agents and host immune mechanisms compared with their planktonic counterparts. This article reviews how microorganisms form biofilms and the mechanisms of protection against antimicrobial agents and the host immune system provided by biofilms. Also discussed are innovative strategies for the diagnosis of biofilm-associated infection and novel approaches to treatment and prevention of medical device-associated infections.

Itch is a common sensory experience that is prevalent in patients with inflammatory skin diseases, as well as in those with systemic and neuropathic conditions. In patients with these conditions, itch is often severe and significantly affects quality of life. Itch is encoded by 2 major neuronal pathways: histaminergic (in acute itch) and nonhistaminergic (in chronic itch). In the majority of cases, crosstalk existing between keratinocytes, the immune system, and nonhistaminergic sensory nerves is responsible for the pathophysiology of chronic itch. This review provides an overview of the current understanding of the molecular, neural, and immune mechanisms of itch: beginning in the skin, proceeding to the spinal cord, and eventually ascending to the brain, where itch is processed. A growing understanding of the mechanisms of chronic itch is expanding, as is our pipeline of more targeted topical and systemic therapies. Our therapeutic armamentarium for treating chronic itch has expanded in the last 5 years, with developments of topical and systemic treatments targeting the neural and immune systems.

Significant advances have been made recent years elucidating antiviral immune mechanisms that protect the host from viral infection. Similarly, our understanding of how viruses bind, enter, and replicate within host cells has continued to grow. Yet, viruses continue to take a toll on human health. The influence of chemicals in the environment is among key factors that influence outcomes of viral infection. There is a growing appreciation of the effects that exogenous environmental chemical exposures have on the immune system and antiviral immunity. Epidemiological studies have linked a variety of chemical exposures to poorer health, increased incidence of infection, and worsened vaccine responses. However, the mechanisms that govern these associations are not well understood, limiting our ability to predict or mitigate the effects of environmental exposures on public health. This brief review focuses on recent advances in the field, highlighting novel in vitro and in vivo findings informed by past foundational studies. Furthermore, current information suggests avenues of investigation that have yet to be explored, but which will significantly impact on our understanding about how environmental exposures impact viral defenses, vaccine efficacy, and the spread of contemporary and emerging viral pathogens.

Inflammatory processes have been shown to play an important role in the mechanisms involved in the pathogenesis of hypertension. Innate and adaptive immune responses participate in BP elevation and end-organ damage. Here, we discuss recent studies focusing on novel inflammatory and immune mechanisms that play roles in BP elevation. Different subpopulations of cells involved in innate and adaptive immune responses, such as dendritic cells, monocytes/macrophages and NK cells, on the one hand, and B and T lymphocytes, on the other, contribute to the vascular and kidney injury in hypertension. Unconventional innate-like T cells such as γδ T cells also participate in hypertensive mechanisms by priming both innate and adaptive immune cells, contributing to trigger vascular inflammation and BP elevation. These cells exert their effects in part via production of various cytokines including pro-inflammatory IFN-γ and IL-17 and anti-inflammatory IL-10. The present review summarizes some of these immune mechanisms that participate in the pathophysiology of hypertension. LINKED ARTICLES: This article is part of a themed section on Immune Targets in Hypertension. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.12/issuetoc.

Objective: To highlight the inflammatory and immunological mechanisms involved in depression and psoriasis. Methods: A comprehensive literature search was performed in various databases, in total 145 studies were selected. Results: Depression and psoriasis have an association. Immune mechanisms -the actions of tumor necrosis factor-a, interleukin 1 (IL-1), IL-2, IL-10, IL-22, IL-17, interferon-7, IL-1ß, prostaglandin E2, C-reactive protein, IL-6, and IL-8 etc.-, and some genetic changes are involved. Conclusions: A possible bidirectional relationship of psoriasis and major depression exists; i.e. the depression leads to psoriasis, and psoriasis leads to depression. We recommend more studies in the future to get a deeper and better understanding about this relationship. RESUMEN Objetivo: Poner de relieve los mecanismos inflamatorios e inmunológicos involucrados en la depresión y la psoriasis. Métodos: Se realizó en varias bases de datos una búsqueda bibliográfica completa; en total se incluyeron 145 estudios. Resultados: Hay asociación entre depresión y psoriasis y están involucrados mecanismos inmunitarios -las acciones del factor de necrosis tumoral alfa, las interleucinas (IL) 1, 2, 10, 22 y 17, el interferón gamma, la IL-1ß, la prostaglandina E2, la proteína C reactiva, la IL-6 y la IL-8, etc. - y algunos cambios genéticos. Conclusiones: Hay una posible relación bidireccional entre psoriasis y depresión, es decir, la depresión lleva a psoriasis y la psoriasis lleva a depresión. Se recomiendan más estudios en el futuro para obtener una comprensión más profunda y mejor sobre esta relación.

The present study, performed in Dahl salt-sensitive (SS) and SS- Rag1−/− rats lacking T and B lymphocytes, tested the hypothesis that immune cells amplify salt-sensitive hypertension and kidney damage in response to a high-protein diet. After being weaned, SS and SS- Rag1−/− rats were placed on an isocaloric, 0.4% NaCl diet containing normal (18%) or high (30%) protein. At 9 wk of age, rats were switched to a 4.0% NaCl diet containing the same amount of dietary protein and maintained on the high-salt diet for 3 wk. After being fed the high-salt diet, SS rats fed high protein had amplified hypertension and albumin excretion (158.7 ± 2.6 mmHg and 140.8 ± 16.0 mg/day, respectively, means ± SE) compared with SS rats fed normal protein (139.4 ± 3.6 mmHg and 69.4 ± 11.3 mg/day). When compared with the SS rats, SS- Rag1−/− rats fed high protein were protected from exacerbated hypertension and albuminuria (142.9 ± 5.8 mmHg and 66.2 ± 10.8 mg/day). After 3 wk of the high-salt diet, there was a corresponding increase in total leukocyte infiltration (CD45+) in the kidneys of both strains fed high-protein diet. The SS- Rag1−/− rats fed high-protein diet had 74–86% fewer CD3+ T lymphocytes and CD45R+ B lymphocytes infiltrating the kidney versus SS rats, but there was no difference in the infiltration of CD11b/c+ monocytes and macrophages, suggesting that the protective effects observed in the SS- Rag1−/− rats are specific to the reduction of lymphocytes. With the SS- Rag1−/− rats utilized as a novel tool to explore the effects of lymphocyte deficiency, these results provide evidence that adaptive immune mechanisms contribute to the exacerbation of salt-induced hypertension and renal injury mediated by increased dietary protein intake.

The review summarizes contemporary literature data on mechanisms of immune respose to development of occupational lung diseases due to dust. Experimental data are compared to results of clinical examinations of workers engaged into main occupations of coal extracting industry. The authors demonstrate universal pathogenetic immune mechanisms underlying formation of lung diseases due to dust, and specific reactions associated with duration of antigen intake by the body.

Oral immunotherapy (OIT) has demonstrated reproducibly successful desensitization in patients with food allergy completing clinical trials and, in some studies, sustained unresponsiveness. These clinical outcomes have been associated with characteristic modifications in the allergen-specific immune response, but a detailed synthesis of OIT's mechanisms of action is lacking. In this rostrum we review the current evidence regarding the human immune response to OIT, explore possible mechanisms, and identify knowledge gaps for future research.

Infections occur commonly after stroke and are strongly associated with an unfavourable functional outcome of these patients. Approaches for effective management of poststroke infection remain scarce, presenting an urgent need for preventive anti-infection strategies for patients who have suffered a stroke. Emerging evidence indicates that stroke impairs systemic immune responses and increases the susceptibility to infections, suggesting that the modification of impaired immune defence could be beneficial. In this review, we summarised previous attempts to prevent poststroke infections using prophylactic antibiotics and the current understanding of stroke-induced immunosuppression. Further elucidation of the immune mechanisms of stroke will pave the way to tailored design of new treatment to combat poststroke infection via modifying the immune system.

The paper gives an update on the pathogenetic role of viral infection and immune mechanisms in the development of cardiac dilatation at the cellular, ultrastructural, and molecular levels. Particular attention is given to the discussion of the possible role of herpesvirus infection in the mechanisms of cardiomyocyte damage with the direct or indirect impact of viral infection through immunoinflammatory responses. Data on the protective and damaging action of a number of cytokines in the immunopathogenesis of viral myocarditis are considered.Представлены современные сведения о патогенетической роли вирусной инфекции и иммунных механизмов в развитии дилатации сердца на клеточном, ультраструктурном и молекулярном уровнях. Особое внимание уделяется обсуждению возможной роли герпесвирусной инфекции в механизмах повреждения кардиомиоцитов при непосредственном влиянии вирусной инфекции или опосредованном действии через иммуновоспалительные реакции. Рассматриваются данные о протективном и повреждающем действии ряда цитокинов в иммунопатогенезе вирусного миокардита.

Rickettsiae are small intracellular bacteria that can cause life-threatening febrile diseases. Rickettsioses occur worldwide with increasing incidence. Therefore, a vaccine is highly desired. A prerequisite for the development of a vaccine is the knowledge of the immune response against these bacteria, in particular protective immunity. In recent years murine models of rickettsial infections have been established, and the study of immune response against rickettsiae in mice provided many new insights into protective and pathological immune reactions. This review summarizes the current knowledge about immune mechanisms in protection and pathology in rickettsial infections.

The immune response is a key factor in the fight against HPV infection and related cancers, and thus, HPV is able to promote immune evasion through the expression of oncogenes. In particular, the E5 oncogene is responsible for modulation of several immune mechanisms, including antigen presentation and inflammatory pathways. Moreover, E5 was suggested as a promising therapeutic target, since there is still no effective medical therapy for the treatment of HPV-related pre-neoplasia and cancer. Indeed, several studies have shown good prospective for E5 immunotherapy, suggesting that it could be applied for the treatment of pre-cancerous lesions. Thus, insofar as the majority of cervical, oropharyngeal and anal cancers are caused by high-risk HPV (hrHPV), mainly by HPV16, the aim of this review is to discuss the immune pathways interfered by E5 oncoprotein of hrHPV highlighting the various aspects of the potential immunotherapeutic approaches.

The field of biologic immune modulators is currently mushrooming at a dizzying pace. Although most of these biologics are tested and approved for one or a few indications, their unanticipated side effects and off-label use have contributed significantly to our understanding of basic immune mechanisms, the involvement of cytokines in several apparently nonimmunologic diseases, and the importance of compartmentalized immune responses. In this review we attempt to give a bird's-eye view of the major biologics and to highlight insights and implications derived from their secondary effects and adverse reactions.

Infected organisms can resist or tolerate infection, with tolerance of infection defined as minimizing per-parasite reductions in fitness. Although tolerance is well studied in plants, researchers have only begun to probe the mechanisms and transmission consequences of tolerance in animals. Here we suggest that research on tolerance in animals would benefit from explicitly incorporating behavior as a component of tolerance, given the importance of behavior for host fitness and parasite transmission. We propose two distinct manifestations of tolerance in animals: tissue-specific tolerance, which minimizes fitness losses due to tissue damage during infection, and behavioral tolerance, which minimizes fitness losses by maintaining normal, fitness-enhancing behaviors during infection. Here we briefly review one set of potential immune mechanisms underlying both responses in vertebrate animals: inflammation and its associated signaling molecules. Inflammatory responses, including broadly effective resistance mechanisms like the production of reactive oxygen species, can incur severe costs in terms of damage to a host's own tissues, thereby reducing tissue-specific tolerance. In addition, signaling molecules involved in these responses facilitate stereotypical behavioral changes during infection, which include lethargy and anorexia, reducing normal behaviors and behavioral tolerance. We consider how tissue-specific and behavioral tolerance may vary independently or in conjunction and outline potential consequences of such covariation for the transmission of infectious diseases. We put forward the distinction between tissue-specific and behavioral tolerance not as a definitive framework, but to help stimulate and broaden future research by considering animal behavior as intimately linked to the mechanisms and consequences of tolerance in animals.