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Autoimmunity is defined as an immune response against a self-antigen. This abnormal immune response can lead to tissue damage and to the development of autoimmune disease. From organ-specific autoimmune diseases, such as myasthenia gravis, to non-organ-specific, such as systemic lupus erythematosus, autoimmune diseases represent a heterogeneous group of disorders which affect approximately 6% of the population. The pathogenesis of many autoimmune diseases is complex and remains not completely understood. The aim of this book is to present current knowledge regarding pathogenic mechanisms of autoimmune diseases, clinical aspects of specific autoimmune diseases, like vitiligo, celiac disease and autoimmune liver disease, as well as insights regarding specific therapies.

Autoimmune diseases --- Treatment. --- Autoimmunologic diseases --- Autoimmunity --- Immunologic diseases --- Immunology

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Successful containment of an infection is dependent on both innate and adaptive immune response. Cytokines are essential effectors of both of these systems. In particular, type I interferons (IFN-I) are important components of early innate immunity against an infection. However, the production of IFN-I could serve as a double edge sword, either containing an infection or enhancing susceptibility. For example, IFN-I, which is essential for early containment of viral infections, has been shown to be detrimental to the host during bacterial infections. In fact, recent significant reports have shown that influenza virus induced IFN-I responses can enhance the host susceptibility to secondary bacterial infections. These recent reports highlight the expanding immunoregulatory role of IFN-I in the host immunity. With these recent findings in mind, the aim of this research topic is to welcome novel data, opinion and literature reviews on the newly identified dual functions of IFN-I. This research topic wills focus on the following areas of IFN-I: 1) a detrimental role of IFN-I during primary bacterial infection; 2) a detrimental role of viral infection induced IFN-I during secondary bacterial infections; 3) evolutionary pressure that drove detrimental IFN-I response during primary bacterial infection; and 4) does benefit of IFN-I responses during primary viral infections outweigh the adverse consequences of IFN-I mediated enhanced susceptibility to secondary bacterial infections.

Autoimmunity --- adjuvant --- bacterial and viral infections --- Vaccine --- type I IFN

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In multicellular organisms, states with a high degree of tissue turnover like embryogenesis, development, and adult tissue homeostasis need an instantaneous, tightly regulated and immunologically silent clearance of these dying cells to ensure appropriate development of the embryo and adult tissue remodelling. The proper and swift clearance of apoptotic cells is essential to prevent cellular leakage of damage associated molecular patterns (DAMPs) which would lead to the stimulation of inflammatory cytokine responses. In addition to the clearance of apoptotic cells (efferocytosis), backup mechanisms are required to cope with DAMPs (HMGB-1, DNA, RNA, S100 molecules, ATP and adenosine) and other intracellular material (uric acid, intracellular proteins and their aggregates) released from cells, that were not properly cleared and have entered the stage of secondary necrosis. Furthermore, under certain pathologic conditions (e.g. gout, cancer, diabetes) non-apoptotic cell death may transiently occur (NETosis, necroptosis, pyroptosis) which generates material that also has to be cleared to avoid overloading tissues with non-functional cellular waste. Efficient efferocytosis is therefore indispensable for normal tissue turnover and homeostasis. The characterization of various signalling pathways that regulate this complex and evolutionary conserved process has shed light on new pathogenetic mechanisms of many diseases. Impaired clearance promotes initiation of autoimmunity as well as the perpetuation of chronic inflammation, but may also foster anti-tumor immunity under certain microenvironmental conditions. Immunological tolerance is continuously being challenged by the presence of post-apoptotic remnants in peripheral lymphoid tissues. Besides the autoimmune phenotype of chronic inflammatory rheumatoid disorders a plethora of pathologies have been associated with defects in genes involved in clearance, e.g. atherosclerosis, cancer, gout, diabetes, some forms of blindness, neuropathy, schizophrenia and Alzheimer’s disease.

Immunology. --- Autoimmunity --- NETs --- Efferocytosis --- Inflammation --- cell-remnants --- Phagocytosis --- Apoptosis --- Cancer --- Asthma --- Autoimmunity --- NETs --- Efferocytosis --- Inflammation --- cell-remnants --- Phagocytosis --- Apoptosis --- Cancer --- Asthma

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Increasing age has been associated with an insufficient protection following vaccination and an increased incidence and severity of infectious diseases. The predicted acceleration of global population aging will accentuate the need to understand the mechanisms that drive the age-related decline of the immune system and to, eventually, identify strategies to lower the burden of infectious diseases in elderly people. One type of immune cell appears to be most dramatically affected by the aging process: T lymphocytes. Age-related changes of the bone marrow and the thymus microenvironment lead to a decreased thymic output of functional, naïve T lymphocytes. As T lymphocytes are key players of the adaptive immune system, this research topic will summarize our current understanding on how aging affects the microenvironmental niches and molecular networks that are important for the generation, survival and function of naïve, memory and effector T lymphocytes. This research topic will also address the impact of aging on the different T lymphocyte lineages, such as regulatory T cells and Th17 cells and how age-related changes of the microenvironment affect organ- and tissue-resident memory T lymphocytes. Eventually, the identification of a set of markers for immunosenescence would facilitate the design and application of more specific therapies and improved vaccines and vaccination strategies for elderly people, thereby increasing life and health span.

Aging. --- T cells --- Autoimmunity --- Cytomegalovirus --- Regulatory T Cell --- Vaccination --- Aging --- Influenza Virus --- biomarker --- health span --- Receptors. --- Autoimmunity --- Cytomegalovirus --- Regulatory T Cell --- Vaccination --- Aging --- Influenza Virus --- biomarker --- health span

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In multicellular organisms, states with a high degree of tissue turnover like embryogenesis, development, and adult tissue homeostasis need an instantaneous, tightly regulated and immunologically silent clearance of these dying cells to ensure appropriate development of the embryo and adult tissue remodelling. The proper and swift clearance of apoptotic cells is essential to prevent cellular leakage of damage associated molecular patterns (DAMPs) which would lead to the stimulation of inflammatory cytokine responses. In addition to the clearance of apoptotic cells (efferocytosis), backup mechanisms are required to cope with DAMPs (HMGB-1, DNA, RNA, S100 molecules, ATP and adenosine) and other intracellular material (uric acid, intracellular proteins and their aggregates) released from cells, that were not properly cleared and have entered the stage of secondary necrosis. Furthermore, under certain pathologic conditions (e.g. gout, cancer, diabetes) non-apoptotic cell death may transiently occur (NETosis, necroptosis, pyroptosis) which generates material that also has to be cleared to avoid overloading tissues with non-functional cellular waste. Efficient efferocytosis is therefore indispensable for normal tissue turnover and homeostasis. The characterization of various signalling pathways that regulate this complex and evolutionary conserved process has shed light on new pathogenetic mechanisms of many diseases. Impaired clearance promotes initiation of autoimmunity as well as the perpetuation of chronic inflammation, but may also foster anti-tumor immunity under certain microenvironmental conditions. Immunological tolerance is continuously being challenged by the presence of post-apoptotic remnants in peripheral lymphoid tissues. Besides the autoimmune phenotype of chronic inflammatory rheumatoid disorders a plethora of pathologies have been associated with defects in genes involved in clearance, e.g. atherosclerosis, cancer, gout, diabetes, some forms of blindness, neuropathy, schizophrenia and Alzheimer’s disease.

Immunology. --- Autoimmunity --- NETs --- Efferocytosis --- Inflammation --- cell-remnants --- Phagocytosis --- Apoptosis --- Cancer --- Asthma