| Literature DB >> 7527820 |
G C MacDonald1, V N Kakkanaiah, E S Sobel, P L Cohen, R A Eisenberg.
Abstract
Mice homozygous for gld develop an autoimmune syndrome characterized by hypergammaglobulinemia, massive accumulation of abnormal T cells and the production of autoantibodies. Previous studies in our laboratory have shown that reconstitution of lethally irradiated B6/gld recipients with a mixture of normal and gld bone marrow (BM) suppresses the gld-induced syndrome. In this report we extend this observation by demonstrating that the depletion of normal Thy-1+ cells, but not normal B cells, restores gld disease in mixed BM chimeras congenic for Thy-1 and IgH alleles. These results strongly suggest that normal T cells suppress the development of gld-related abnormalities. It is probable that the mechanism by which normal Thy-1+ cells mediate the suppression is Fas ligand dependent.Entities:
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Year: 1995 PMID: 7527820
Source DB: PubMed Journal: J Immunol ISSN: 0022-1767 Impact factor: 5.422