T-cells primarily mediate SKG arthritis . Transfer of spleen and lymph node T-cells, CD4+ T-cells in particular, from arthritic SKG mice produces similar arthritis in T-cell-deficient athymic BALB/c nude mice, whereas transfer of the sera from the same SKG mice does not. Transfer of thymocyte suspensions from arthritic or non-arthritic young SKG mice also elicits severe arthritis in BALB/c nude mice and T/B cell-deficient C.B-17 SCID mice. In addition, transfer of T-cell-depleted bone marrow (BM)-cell suspensions from SKG mice produces severe arthritis in SCID mice, but not in SCID mice thymectomized prior to the transfer. Taken together, the RA-like arthritis in SKG mice is a bona fide autoimmune disease mediated by apparently joint-specific CD4+ T-cells, in accord with the infiltration of CD4+ T-cells to subsynovial tissue in SKG arthritis. The SKG thymus is continuously generating arthri-togenic autoimmune T-cells. Furthermore, SKG bone marrow cells give rise to such arthritogenic T-cells through the normal thymic environment, indicating that the arthritogenic abnormality in SKG mice is T-cell-intrinsic.
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