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Dendritic Cell Control of Immune Responses

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889198689 Year: Pages: 121 DOI: 10.3389/978-2-88919-868-9 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-01-19 14:05:46
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Dendritic cells (DC) are among the first cells to encounter pathogens and damage in peripheral tissues and, upon activation, DC migrate to lymph nodes where they activate and educate T cells to initiate and shape the immune response. DC present pathogen-derived antigen to T cells and drive T cell differentiation into particular effector cells through the expression and secretion of co-stimulatory molecules and cytokines respectively. The study of DC biology has included the identification of multiple DC subsets in tissues and lymphoid organs, the differentiation and plasticity of DC subsets, the functional consequences of DC interaction with pathogen, control of DC migratory properties and the impact of DC on T cell activation and differentiation. In recent years sophisticated systems biology approaches have been developed to deepen our understanding of DC function. These studies have identified differences between DC subsets located in various tissues and critical factors that drive the outcome of the interaction between DC and T cells. DC are currently being used in in various clinical therapeutic settings, including as vaccines for cancer and autoimmune disease. A clear understanding of DC factors that contribute to specific immune responses is vital to the success of DC based therapies. This research topic will give a comprehensive overview of current issues in DC biology and provides an update on the clinical uses of DC in the therapy of autoimmunity and cancer.

Tumor Cell/Dendritic Cell Interactions and the Influence of Tumors on Dendritic Cell-mediated Anti-Tumor Immune Responses and Dendritic Cell-Based Tumor Immunotherapies

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889192458 Year: Pages: 160 DOI: 10.3389/978-2-88919-245-8 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology --- Oncology
Added to DOAB on : 2015-11-16 15:44:59
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Significant efforts over the last two decades have been made to better understand the factors that control DC maturation and activation and the impact of these processes on overall host immunity. In addition to the well-characterized role of DC in the induction of immunity to pathogens, a role for these cells as critical regulators of anti-tumor immune responses has more recently become apparent. These findings have generated interest in understanding how tumor/DC interactions impact the quality of anti-tumor immune responses, and they have contributed to increased enthusiasm for a variety of DC-based cancer immunotherapies. Such strategies have included DNA- or peptide-based vaccines that involve uptake and processing of tumor antigens by endogenous DC in cancer patients or the administration of tumor antigen-loaded exogenous DC-based vaccines. Additionally, many adjuvant, cytokine, and monoclonal antibody therapies aim either to enhance the immunostimulatory capacity of endogenous DC or to supplement the activity of these cells by targeting costimulatory receptors on T cells. Despite the promise of such therapeutic approaches for cancer treatment, their success is often limited, and much remains to be understood about how tumors influence DC function and the quality of DC-mediated immune responses. Tumor/DC interactions have therefore become an increasingly active area of investigation, and many studies have described effects of tumors on DC phenotype and function that include an accumulation of immature DC within tumors, tumor-altered differentiation of DC precursors into myeloid-derived suppressor cells, and the generation of tumor-associated DC with immunoregulatory properties. As this field moves forward, it will be important to gain mechanistic insights into the basis for both tumor-mediated DC dysfunction as well as the induction of either suboptimal or immunosuppressive adaptive anti-tumor immune responses by tumor-associated DC. Progress in these areas of tumor immunology will greatly improve our understanding of the factors that contribute to effective DC-mediated anti-tumor immune control versus DC-associated anti-tumor immune dysfunction and subsequent tumor immune escape. Such information is vital for improving current and developing novel immunotherapeutic strategies for interfering with tumor-associated DC dysfunction and enhancing the functional quality of endogenous DC in cancer patients as well as the efficacy of exogenous DC-based anti-tumor vaccines. The articles contained within this special issue highlight these important topics and bring focus not only to our current understanding of tumor/DC interactions but also to major areas of investigation that remain ongoing in this field.

Autoimmuno-Anti-Tumour Immunity (AATI) - Understanding the Immune Responses against "Self" & "Altered-self"

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889451906 Year: Pages: 174 DOI: 10.3389/978-2-88945-190-6 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2017-10-13 14:57:01
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The brief description of tumours being “wounds that do not heal” by Dr Harold F. Dworak nearly three decades ago (N Engl J Med 1986) has provided not only a vivid illustration of neoplastic diseases in general but also, in retrospect conceptually, a plausible immunological definition of cancers. Based on our current understanding in the field, it could have even a multi-dimensional meaning attached with. This relates to several important issues which need to be addressed further, i.e. in terms of a close link between chronic inflammation and tumourigenesis widely observed; clinical and experimental evidence of immunity against tumours versus the highly immunosuppressive tumour microenvironment being associated; and their underlying immunological mechanisms, oncogenic basis, as well as the true causal relationship in question. Recent findings from studies into the pathogenesis of autoimmunity and, more importantly, the mechanisms which protect against it, have offered some new insights for our understanding in this direction. Chronic or persistent autoimmune-like inflammatory conditions are evidently associated with tumor development. The important question is about their true causal relationship. Chronic or persistent inflammation has been shown to contribute directly to tumour development by triggering neoplastic transformation and production of inflammatory mediators which could promote cancer cell survival, proliferation and invasion. On the other hand, tumours are mutated self-tissue cells to which the host immune system is largely tolerized otherwise. Although the mutations may give rise to the expression of tumour-specific antigens (TSA) or tumour-associated antigens (TAA), most of these TSAs/TAAs are found to be poor immunogens. The ongoing inflammatory conditions may therefore reflect a desperate attempt of the host immune system to mount anti-tumour responses, though ineffectively, being a consequence of the continuous yet largely futile triggering by those poorly immunogenic TSAs/TAAs. Furthermore, during autoimmune or overtly persistent immunological responses, many regulatory mechanisms are triggered in the host in attempts to limit the ongoing harmful inflammatory reactions. Such a negative feedback regulation is known to be crucial in preventing normal individuals from immune-mediated diseases. As a result of the negative feedback loop, however, an excessive production of anti-inflammatory or immunosuppressive molecules followed by the exhaustion of the immune effector cells may instead lower the ability of the host immune system to mount specific anti-tumor responses, allowing the escape of tumour or mutated cells from immunosurveillance. This may also help to explain why the most effective way to enhance host immunity against cancer is by targeting the negative arm of immune regulation. In this Frontiers Research Topic, we aim to gather current views from experts in these inherent overlapping fields of oncology, autoimmunity and tumour immunology, and to make them available to our potential readership who may be particularly interested in this cutting-edge area. By understanding how the immune system is normally regulated, why dysregulation of which may cause the immunological-oncological related diseases, we also encourage further discussions as to how the so-called "self-reactivity" (autoimmune responses) can be alternatively switched on and redirected, immunologically or molecularly, for effective cancer treatment.

Apoptotic Cell Clearance in Health and Disease

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889456888 Year: Pages: 294 DOI: 10.3389/978-2-88945-688-8 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2019-01-23 14:53:43
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Clearance of apoptotic cells is essential for proper development, homeostasis and termination of immune responses in multicellular organisms. Thus, cellular and molecular players taking part in the sequential events of this process are of great interest. Research in the last 20 years has indicated that specific ligands and receptors take part in the attraction of immune cells toward apoptotic targets and in the interactions between apoptotic cells and professional as well as non-professional phagocytes that engulf them. Moreover, phagocytosis of apoptotic cells (efferocytosis) leads to significant phenotypic changes in the engulfing cells suggesting that it is a major fate-determining event for phagocytes. Particularly, efferocytosis has an important impact on the inflammation-resolution axis as well as embryonic development and tissue morphogenesis. Deficiencies in these processes can result in health threats, such as autoimmunity, atherosclerosis, bone loss, obesity, infertility, neurodegeneration, fibrosis and cancer. This eBook brings together 24 original research and review manuscripts that cover various aspects of apoptotic cell removal during normal development and homeostasis as well as in tumorigenesis and regenerative processes following injury.

The Coevolution of IDO1 and AhR in the Emergence of Regulatory T Cells in Mammals

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197293 Year: Pages: 89 DOI: 10.3389/978-2-88919-729-3 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-04-07 11:22:02
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Indoleamine 2,3-dioxygenase (IDO1) is an ancestral enzyme that, initially confined to the regulation of tryptophan availability in local tissue microenvironments, is now considered to play a wider role that extends to homeostasis and plasticity of the immune system. Thus IDO biology has implications for many aspects of immunopathology, including viral infections, neoplasia, autoimmunity, and chronic inflammation. Its immunoregulatory effects are mainly mediated by dendritic cells (DCs) and involve not only tryptophan deprivation but also production of kynurenines that act on IDO- DCs, thus rendering an otherwise stimulatory DC capable of regulatory effects, as well as on T cells. The aryl hydrocarbon receptor (AhR) is a ligand-operated transcription factor originally recognized as the effector mediating the pathologic effects of dioxins and other pollutants. However, it is now well established that AhR activation by endogenous ligands can produce immunoregulatory effects. The IDO1 mechanism appears to have been selected through phylogenesis primarily to prevent overreacting responses to TLR-recognized pathogen-associated molecular patterns, and only later did it become involved in the response to T cell receptor-recognized antigens. As a result, in mammals, IDO1 has become pivotal in fetomaternal tolerance, at a time when regulatory T cells emerged to meet the same need, namely protecting the fetus. IDO1 and regulatory T (Treg) cells may have then coevolved to broaden their function well beyond their initial task of protecting the fetus, such that, in acquired immunity, IDO1 (with its dual enzymic and signaling function) has turned into an important component of the peripheral generation and effector function of regulatory T cells. AhR, in turn, which has a role in regulatory T-cell generation, is presumed to have evolved from invertebrates, where it served a ligand-independent role in normal development processes. Evolution of the receptor in vertebrates resulted in the ability to bind structurally different ligands, including xenobiotics and microbiota-derived catabolites. Considering the inability of invertebrate AhR homologs to bind dioxins, the adaptive role of the AhR to act as a regulator of xenobiotic-metabolizing enzymes may have been a vertebrate innovation, to later acquire an additional immune regulatory role by coevolutive pressure in mammals by IDO1 and regulatory T cells. Thus an entirely new paradigm in immunology, and more specifically in immune tolerance, is the coevolution of three systems, namely, the IDO1 mechanism, AhR-driven gene transcription, and T-cell regulatory activity, that originating from the initial need of protecting the fetus in mammals, have later turned into a pivotal mechanism of peripheral tolerance in autoimmunity, transplantation, and neoplasia.

The Second Life of Natural Killer (NK) Cells

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889455461 Year: Pages: 118 DOI: 10.3389/978-2-88945-546-1 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2019-01-23 14:53:42
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Natural Killer (NK) cells are innate lymphocytes, now recognized as members of a larger family of “Innate lymphoid cells” (ILCs). Both murine and human NK cells are well characterized effector cells with cytotoxic as well as cytokine production ability which mainly react in response to microbial and cell stress stimuli, thus playing a central role in the defense against pathogen infection, in tumor surveillance and in regulating immune homeostasis. Despite these established concepts, our understanding of the complexity of NK cells, also in view of their developmental and functional relationship with other ILC subsets, is only recently emerging. This Research Topic highlights the recent advances in NK cell (and ILC) research in human and mouse from basic research to clinical applications.

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