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Red plaster mask representing the twisting of the immune system, normally a protector of health and well being (right side of mask) into an instrument of destruction and dysregulation (left side). Half of this month's issue (pages 755 to 822) is focused on the new theoretical frameworks that have arisen to explain autoimmunity and recent developments in treatment of autoimmune disorders. Additional features are available free on Nature Immunology's website (immunol.nature.com). Mask by Christopher Cassidy.
The pathogenesis of multiple sclerosis consists of an inflammatory and neurodegnerative phase. Better understanding of these stages has aided the development of specific therapeutic targets.
B cells can regulate many aspects of immune reactivity, as well as differentiate into antibody-producing cells. In SLE, a systemic autoimmune disease, recent research suggests enhanced B cell function is the defining pathogenic event.
Type 1 diabetes is preventable in animal models and predictable in humans. The increase in our knowledge of basic immunology has allowed the initiation of large-scale clinical efforts to prevent diabetes.
Graves' disease and other autoimmune syndromes affecting the thyroid are the archetypes of organ-specific autoimmunity. Despite intensive research, the relative contribution of genetic and environmental factors to disease pathogenesis is not clear. Here, the latest developments in understanding the determinants of these diseases are discussed.
Autoimmune diseases are more prevalent in women than men. A new interest in understanding the biology of this difference as well as funding opportunities have focused attention on research priorities in sex differences.
Differences in multiple sclerosis patient's disease and their responses to standard drugs indicate that today's therapies need to be more individualized. It is proposed that gene expression profiling in conjunction with magnetic resonance imaging be used to optimize future treatment approaches.
The development of increasingly powerful methods to stimulate anti-tumor immune responses carries the risk of breaking tolerance to self and causing autoimmune pathology. How concerned should we be?
In early July 2001 a small meeting was held in Baltimore on the associations of lymphomas with autoimmune conditions. Topics ranged from the effects of defective apoptosis to questions of antigen-drive lymphoproliferation.
Successful passage through several developmental checkpoints determines whether thymocytes survive, proliferate or differentiate. New data show that Wnt-frizzled–induced activation of TCF-1 or Lef-1, via their coactivator β-catenin, is critical during TCRB and TCRA gene rearrangement in thymocytes.
Individual lymphocytes express antigen receptors of a singular specificity. How this process, known as allelic exclusion, is established and maintained is unknown. Differences in subnuclear localization appear to contribute to enforcement of monoallelic receptor expression.
The era of genomic-wide sequence analysis promises to yield new insights in global regulatory gene control. Comparative genome studies have identified a critical regulator of TH2 cytokine expression.
Although some cellular responses induced by TLRs are abolished in MyD88-deficient mice, TLR4, unlike TLR9, can still induce activation of NF-κB and MAPKs. The discovery of a cytoplasmic adapter protein for TLR4, called TIRAP, helps explain this phenomenon.
Dendritic cells can prime naïve lymphocytes. New data show how dendritic cells provide early activation cues by expression of IL-2, which may greatly enhance both T and B cell responses.
The mechanisms that cause autoimmune disorders are not fully worked out, in spite of intense effort. This focus thoroughly examines recent clinical and research progress in understanding autoimmunity.