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Proceedings of the Seventh International Conference held in New Port Beach, California, February 6-8, 1998
This volume reviews the most recent advances in the understanding of cellular and molecular mechanisms for immune responses and immune regulation. The books editor, Dr. Zhang, is well-known internationally, particularly in the field of multiple sclerosis and T-cell vaccination as a potential treatment of multiple sclerosis. He has much experience and expertise in both basic and clinical aspects of autoimmune disease.
The Janeway's Immunobiology CD-ROM, Immunobiology Interactive, is included with each book, and can be purchased separately. It contains animations and videos with voiceover narration, as well as the figures from the text for presentation purposes.
Dendritic cells (DCs) play a critical role in immune system, as they are necessary both for innate and adaptive immunity. According to their function, dendritic cells can be classified in immune tolerogenic or inflammatory DCs. DCs have been shown to regulate T cell-mediated immune responses and lead to immune tolerance and autoimmunity. For example, immune-tolerogenic DCs facilitate the development of regulatory T cells and inhibit T helper 17-mediated autoimmunity in mice with experimental autoimmune encephalomyelitis. Moreover, inflammatory DCs activate CD8+ and CD4+ T cells and elicit T cell-mediated inflammatory immune responses in vivo. However, the molecular and cellular mechanisms underlying DC-mediated immune tolerance and autoimmunity are still obscure.
Inflammation is critical for the development of many complex diseases and disorders including autoimmune diseases, metabolic syndrome, neurodegenerative diseases, cancers, and cardiovascular diseases. Inflammation comes as two types: chronic inflammation, which can be defined as a dysregulated form of inflammation, and acute inflammation, which can defined as a regulated form. Because of its special role in the aforementioned diseases, establishing methods to control chronic inflammation is important for developing cures and treatments. One challenge for this purpose has been the ability to distinguish chronic and acute inflammation based on molecular biology diagnostics. Thus, this Research Topic is focused on articles that can shed some new light on the molecular mechanisms responsible for the development of chronic inflammation and its related conditions.
Ever since Regulatory T cells (T-Regs) were first defined as peripheral CD4+ T cells that express the interleukin-2 (IL-2) receptor alpha chain (IL-2Ra), there have been intensive efforts to determine the molecular mechanisms whereby this minor subset of CD4+ T cells (~ 5-10%) nonspecifically suppresses all potential effector T cells, whether reactive to self or non-self antigens. Multiple possible molecular mechanisms have been implicated, including the scavenging of IL-2 via the expression of high densities of IL-2Rs, the inhibition of antigen presentation via CTLA-4 molecules leading to decreased IL-2 production, the activation of intracellular cAMP thereby suppressing both IL-2 production and action, and the production of suppressive cytokines such as IL-10 and Tumor Growth Factor-beta, to list a few. However, the field has thus far failed to come to a consensus, such that some investigators have now asserted that many molecular mechanisms may be operative, in fact that perhaps all of the described mechanisms may account for the suppressive effects of these cells, acting either simultaneously or sequentially. Thus, this Research Topic is focused on articles that can shed some new light on the molecular mechanisms responsible for T-Reg immunosuppression.