Regulation by @entity2902 + lymphocytes of autoantigen-specific T-cell responses in XXXX .

@entity1 @entity6306 @entity8 @entity7860 @entity2902 @entity792
BACKGROUND: Goodpasture's, or anti-glomerular basement membrane (GBM), disease is unusual among @entity792 in that it rarely follows a relapsing-remitting course. Moreover, untreated, autoantibodies disappear spontaneously after 1 to 3 years and, following treatment, autoreactive T cells diminish in frequency. This suggests that operational tolerance toward the autoantigen is reestablished. However, the mechanisms underlying this have remained unclear. Recent data have suggested that a population of regulatory T lymphocytes can suppress both autoimmune and alloimmune responses in animal models and are present in normal individuals. However, to date, they have not been demonstrated to play a role in @entity1 @entity8 . METHODS: We studied the role of regulatory @entity2902 + cells in suppressing T-cell responses to the Goodpasture autoantigen in nine @entity1 with @entity7860 . RESULTS: At the time of acute presentation, there was no evidence of a regulatory cell population. However, from 3 months onward a population emerged, capable of suppressing the response to the Goodpasture autoantigen. Following depletion of @entity2902 + cells, the frequencies of autoreactive-, GBM-, or collagen alpha 3(IV)NC1-specific T cells were significantly increased (P = 0.031 by paired t test), with five of seven (71%) convalescent @entity1 and no acute @entity1 demonstrating regulation. CONCLUSION: These data demonstrate that, in @entity7860 , regulatory @entity2902 + T cells play a role in inhibiting the autoimmune response. Their emergence and persistence may underlie the "single hit" nature of this condition. Understanding the conditions required for the development and propagation of these cells would allow development of novel therapeutic strategies for inducing @entity6306 in @entity792 .
