THE ROLE OF THE B-CELLS IN THE ADOPTIVE TRANSFER OF COLLAGEN-INDUCED ARTHRITIS FROM DBA 1 (H-2(Q)) TO SCID (H-2(D)) MICE/

Collagen-induced arthritis (CIA) can be transferred from DBA/1 to SCID mice when native type II, collagen (CII) is administered together wit h spleen cells, arthritis appearing some 14 days after cell transfer. In the present study, we demonstrate that both donor T- and B-lymphocy te populations play a role in this model, and that arthritis arises in SCID recipients of either murine or bovine native CII. Furthermore, t he requirement for administration of soluble native CII can be replace d by subarthritogenic doses of serum from Wistar rats with CIA. In thi s case a fully developed arthritis appears as early as 2 days after ce ll transfer. However, protein G-purified IgG from CIA rat serum togeth er with splenocytes from arthritic DBA/1 mice does not transfer arthri tis. A key role of B cells in this model appears to be the production of a humoral arthritogenic factor since arthritis can be successfully transferred to SCID mice by CIA rat serum administered together with a B cell-depleted splenocyte population consisting of T cells and donor -histocompatible antigen-presenting cells. By contrast, transfer of di sease cannot be achieved by co-administration of CIA rat serum and pur ified donor T cells, indicating that the presence of donor antigen-pre senting cells is a requirement for adoptive transfer of arthritis. We propose that joint damage initiated by arthritogenic product(s) of the B cell lineage releases soluble antigens that are presented to T cell s which perpetuate the disease. The finding that arthritis can be gene rated in SCID recipients of CIA rat serum together with splenocytes fr om non-arthritic DBA/1 mice immunized with denatured CII supports the hypothesis that T cells with specificity for denatured joint component s perpetuate disease initiated by humoral factors.