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Differential Control of Autoantibodies and Lymphoproliferation by Fas Ligand Expression on CD4⁺ and CD8⁺ T Cells In Vivo^{1 ,2}

Michael A. Maldonado^3,*, Glen C. MacDonald^3,, Vellalore N. Kakkanaiah, Karamarie Fecho, Mark Dransfield, Debora Sekiguchi^*, Philip L. Cohen^* and Robert A. Eisenberg^4,*

^* Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104; and Departments of Medicine and Microbiology/Immunology, University of North Carolina, Chapel Hill, NC 27599

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.

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