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In vitro peptide stimulation of allergen-reactive T-helper type 1 and type 0 cells, in the absence of costimulatory signals, induces anergy that is accompanied by the modulation of cell surface phenotype and changes in cytokine production. In experimental animal models, the administration of...
Many intracellular proteins and nucleic acids, that are involved in important biosynthetic pathways, are targeted by autoantibodies occurring spontaneously in the sera of patients with systemic autoimmune diseases. Frequently, the autoantigens are assembled into multicomponent complexes...
The study of autoimmune disease in the context of T-helper type 1 (Th1) and T-helper type 2 (Th2) CD4 + T-cell responses demonstrates that the relative contribution of either T-cell type to the development of a particular autoimmune response can influence whether or not this response leads to...
Self-reactive B cells are eliminated in a series of checkpoints that are triggered by antigen binding. Recent reports have shown that in addition to the processes of elimination at the immature B-cell stage, B-cell anergy and regulation of T-cell help, self-reactive cells are also controlled by...
Controlling the IgE response at either the synthesis level or the effector phase should have a profound impact on the allergic cascade. For more than a decade, researchers have focused on ways of interfering with the binding of IgE to its high-affinity receptor on proinflammatory cells. Several...
In the past year, the major advances in understanding the genetics of autoimmune disease in both man and mouse have been made as a result of using the positional cloning approach. Construction of congenic mouse strains, and, in humans, the exploitation of linkage disequilibium between very...
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