A novel mouse with B cells but lacking serum antibody reveals an antibody-independent role for B cells in murine lupus.

J.Exp.Med. 189:1639.

Chan, O.T., L.G. Hannum, A.M. Haberman, M.P. Madaio, and M.J. Shlomchik. 1999

These authors have performed a series of studies delineating the role of B cells in a mouse model of SLE. The MRL/lpr strain of mice spontaneously develops a spectrum of pathology including glomerulonephritis, interstitial nephritis, vasculitis and skin disease that closely resembles human SLE. In a previous study the authors showed that if these mice were rendered genetically deficient in B lymphocytes, they became resistant to the development of lupus (1). In an additional paper, the authors present similar findings in MRL mice that are not deficient in Fas (2).
In the present study the authors have engineered mice that express immunoglobulin on the surface of their B lymphocytes but are unable to secrete immunoglobulin. In this way the role of secreted autoantibodies in lupus can be dissected.
The authors find that mice that are unable to secrete antibody are still susceptible to lupus-like disease characterized by interstitial nephritis and vasculitis. This suggests that B cells have a role in the development of lupus beyond the secretion of autoantibodies.
There is an increasing realization of the importance of B lymphocytes as antigen-presenting cells for T lymphocytes in immunized animal models. This study provides evidence that B cells can also act as antigen presenting cells in spontaneous autoimmune disease.
1. Shlomchik, M.J., M.P. Madaio, D. Ni, M. Trounstein, and D. Huszar. 1994. The role of B cells in lpr/lpr-induced autoimmunity. J.Exp.Med. 180:1295.
2. Chan, O.T.M., M.P. Madaio, and M.J. Shlomchik. 1999. B cells are required for lupus nephritis in the polygenic, fas-intact MRL model of systemic autoimmunity. J.Immunol. 163:3592.