Literature DB >> 7527820

In vivo depletion of Thy-1-positive cells originating from normal bone marrow abrogates the suppression of gld disease in normal-gld mixed bone marrow chimeras.

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.

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Year:  1995        PMID: 7527820

Source DB:  PubMed          Journal:  J Immunol        ISSN: 0022-1767            Impact factor:   5.422


  4 in total

Review 1.  Fas- and perforin-independent mechanism of cytotoxic T lymphocyte.

Authors:  K Kajino; Y Kajino; M I Greene
Journal:  Immunol Res       Date:  1998       Impact factor: 2.829

Review 2.  Mechanisms of systemic autoimmunity in murine models of SLE.

Authors:  R Eisenberg
Journal:  Immunol Res       Date:  1998       Impact factor: 2.829

3.  Apoptosis with FasL+ cell infiltration in the periphery and thymus of corrected autoimmune mice.

Authors:  T Kobata; K Takasaki; H Asahara; N M Hong; K Masuko-Hongo; T Kato; S Hirose; T Shirai; N Kayagaki; H Yagita; K Okumura; K Nishioka
Journal:  Immunology       Date:  1997-10       Impact factor: 7.397

Review 4.  Mechanisms of autoimmunity.

Authors:  Robert Eisenberg
Journal:  Immunol Res       Date:  2003       Impact factor: 2.829

  4 in total

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