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Immunomodulatory Effects of Drugs for Treatment of Immune-Related Diseases

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889452880 Year: Pages: 108 DOI: 10.3389/978-2-88945-288-0 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2018-02-27 16:16:44
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More than 90% of diseases possess immunological abnormalities. Disorders such as inflammation, hypersensitivity, autoimmunity and immunodeficiency are simple examples of how the immune system misinterprets its surroundings and goes awry. Multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel diseases, among many others are manifestations of immune cells attacking normal tissues. On the other hand, damping the immune system leads to diseases such as cancer, AIDS, and severe combined immunodeficiency. The last ten years witnessed an explosion in developing drugs that target the immune system. Several novel monoclonal antibodies have been approved for treatment of various diseases confirming that personalized medicine approach is robust in combating diseases. Hence, the future holds great promise for using personalized and targeted medicine rather than generalized medications that, in most circumstances, proven to be ineffective and characteristically exert side effects. Approaches such as generating novel adjuvants that can stimulate the immune system without harmful side effects, targeting inflammatory cytokines and chemokines, harnessing and activating innate immune cells such as natural killer cells or dendritic cells, are examples of future approaches to treat autoimmune diseases, AIDS, and various forms of cancer resulting from chronic inflammation. More recently, targeting immune checkpoint molecules have shown therapeutic response against lung cancer and melanoma. Identifying molecules involved in autophagy is another example of how personalized medicine might help treat patients with refractory asthma and autoimmune diseases. This topic introduces the reader to these novel approaches of manipulating the immune system and developing targeted therapeutic strategies for treatment of various diseases.

Lymphocytes in MS and EAE: More than just a CD4+ World

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453023 Year: Pages: 160 DOI: 10.3389/978-2-88945-302-3 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2018-02-27 16:16:45
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Multiple sclerosis is degenerative disease of the central nervous system (CNS) in which myelin destruction and axon loss leads to the accumulation of physical, cognitive, and mental deficits. MS affects more than a million people worldwide and managing this chronic disease presents a significant health challenge. Multiple lines of evidence indicate that MS is an autoimmune disorder in which immune cells launch an inflammatory attack targeting myelin antigens. Indeed, myelin-reactive T cells and antibodies have been identified in MS patients and in animal models (namely experimental autoimmune encephalomyelitis, or EAE) that recapitulate many features of human disease. Animal model studies have demonstrated that T cells are both necessary and sufficient to initiate and sustain CNS autoimmunity. However, most MS animal models rely on the role played by CD4+ T cells and partially replicate the multiple aspects of MS pathogenesis. Thus, research in the past has focused heavily on the contribution of CD4+ T cells to the disease process; searching PubMed for “MS AND CD4” yields twice the results as corresponding searches for “CD8” or “B cell” and four times that for “NK cells”. While CD4+ T cells may represent the minimum requirement to mediate CNS autoimmunity, it is clear that the immune response underlying human MS is far more complex and involves numerous other immune cells and subsets. This is well illustrated by the observation that MS patients treated with an anti-CD4 depleting antibody did not gain any clinical benefits whereas removal of several lymphocyte subsets using an anti-CD52 depleting antibody has been shown to impede disease progression. In particular, the pathogenic role(s) of non-CD4+ T cell lymphocytes is relatively poorly understood and under-researched, despite evidence that these subsets contribute to disease pathology or regulation. For example, the observed oligoclonal expansion of CD8+ T cells within the CNS compartment supports a local activation. CD8+ T cells with polarized cytolytic granules are seen in close proximity to oligodendrocytes and demyelinated axons in MS tissues. The presence of B cells in inflammatory lesions and antibodies in the CSF have long been recognized as features of MS and Rituximab, a B cell depleting therapy, has been shown to be highly effective to treat MS. Intriguingly, the putative MS therapeutic reagent Daclizumab may function in part through the expansion of a subset of immunoregulatory NK cells. NKT and ?d T cells may also play a role in CNS autoimmunity, given that they respond to lipid antigens and that myelin is lipid-rich. While different animal models recapitulate some of these aspects of human disease, identifying appropriate models and measures to investigate the role of these less well-understood lymphocytes in MS remains a challenge for the field. This Frontiers research topic aims to create a platform for both animal- and human-focused researchers to share their original data, hypotheses, future perspectives and commentaries regarding the role of these less-well understood lymphocyte subsets (CD8+ T cells, B cells, NK cells, NK T cells, ?d T cells) in the pathogenesis of CNS autoimmunity.

Induction of Central Nervous System Disease by the Adaptive Immune Response

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453474 Year: Pages: 141 DOI: 10.3389/978-2-88945-347-4 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology --- Neurology
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Over the last years it has become evident that many neurological diseases of the central nervous system (CNS) are induced by a specific adaptive immune response directed against molecules expressed on CNS-resident cells. Well-recognized examples are anti-N-Methyl-D-Aspartate Receptor (NMDAR) encephalitis which is characterized by the presence of antibodies against neuron-expressed NMDAR, or neuromyelitis optica (NMO), induced by antibodies to astrocyte-expressed aquaporin-4. Many more examples exist, and antibodies, and T or/and B cells have increasingly been associated with CNS disease. Often the symptoms of these diseases have not been typically reported to have an immune aetiology. Beside classical neurological symptoms like ataxia, vision disturbance, and motor or sensory symptoms, these can include cognitive disturbances, behavioral abnormalities, or/and epileptic seizures. Although much has been learned regarding the pathophysiology of prototypic examples of these disorders, there are still major gaps in our understanding of their biology. This may be due to the fact that they are rare diseases, and their therapies are still very limited. This research topic includes contributions addressing the analysis of the adaptive immune response driving disease including target antigens, molecular epitope mapping, and factors involved in the disease pathogenesis such as complement activation cascades, genetic and genomic regulation, as well as environmental triggers. Diagnostic criteria and methods, and treatment are also discussed. The overall aim of the volume is to review progress in our pathophysiological understanding of immune-mediated CNS disorders in order to advance diagnostic and therapeutic approaches, and ultimately improve outcomes for patients.

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