Differential control of autoantibodies and lymphoproliferation by Fas ligand expression on CD4+ and CD8+ T cells in vivo
| Autor: | M A, Maldonado, G C, MacDonald, V N, Kakkanaiah, K, Fecho, M, Dransfield, D, Sekiguchi, P L, Cohen, R A, Eisenberg |
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| Rok vydání: | 1999 |
| Předmět: |
CD4-Positive T-Lymphocytes
Mice Knockout Transplantation Chimera Fas Ligand Protein Membrane Glycoproteins CD8-Positive T-Lymphocytes Lymphocyte Activation T-Lymphocytes Regulatory Autoimmune Diseases Mice Inbred C57BL Mice Mice Congenic T-Lymphocyte Subsets Animals Autoantibodies Bone Marrow Transplantation |
| Zdroj: | Journal of immunology (Baltimore, Md. : 1950). 163(6) |
| ISSN: | 0022-1767 |
| Popis: | We have previously shown that the gld autoimmune syndrome is suppressed in lethally irradiated gld mice reconstituted with a mixture of normal and gld bone marrow (BM). Furthermore, in vivo depletion of normal Thy-1+ cells restores lymphoproliferation and autoantibody production in such chimeras, suggesting that T cells bearing Fas ligand are responsible for correcting the gld defect. In this study, mixed-BM chimeras lacking either normal CD4+ (B6CD4KO-B6gld) or normal CD8+ T cells (B6CD8KO-B6gld) were generated to determine the contribution of the normal T cell subsets to disease suppression. Lymphoproliferation was completely suppressed in B6CD4KO-B6gld chimeras but only modestly in B6CD8KO-B6gld chimeras. On the other hand, both types of mixed-BM chimeras had incomplete effects on the suppression of serum autoantibodies when compared with B6gld reconstituted with isologous BM. These results suggest that both T cell subsets provide Fas ligand to suppress immune cells responsible for autoantibody production; however, CD8+ T cells are mainly responsible for preventing lymphoproliferation. |
| Databáze: | OpenAIRE |
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