Mechanisms of regulation

An open question is how the anti-idiotypic and anti-ergotypic regulatory cells arrest the autoimmune disease process. Specific autoimmune T cells persist in TCV-treated animals, suggesting that effective regulation of disease does not depend on total deletion of the autoimmune effector cells. Indeed, TCV was found to suppress inflammation without inhibiting the production of autoantibodies. The divergent effects of TCV on tissue damage and antibody production may be explained by the Tnl-TH2 dichotomy. TCV has been found to enhance a switch from a proinflammatory THl-type cytokine response to an anti-inflammatory TH2-type cytokine response. Following TCV, the treated animals still respond to the target self antigen; however, instead of producing large amounts of interferon 7 and interleukin 2 (IL-2), the responding T cells produce low amounts of these cytokines and high amounts of IL-4, IL-10 and transforming growth factor 3 (TGFp). The shift in cytokine profile induced by TCV leads, in mice, to the production of immunoglobulin G1 (IgGl) iso-type antibodies to the target self antigens. This shift has been observed both in naked DNA TCV against mouse EAE and in TCR peptide (VDJp) vaccination against spontaneous diabetes in the NOD mouse. It remains to be determined whether TCV works bv inducing existent TH1 clones to change their cytokine output, or by activating dormant clones of Tn2 T cells to suppress the pathogenic TH1 clones. In either case, these findings call attention to the influence of T-T interactions on the cytokine profile of the immune response.

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