Eur J Immunol 2002 Jul;32(7):1939-1946
Svensson L, Abdul-Majid KB, Bauer J, Lassmann H, Harris RA, Holmdahl R.
Medical Inflammation Research, Lund University, Lund, Sweden.
We have investigated the role of B cells in myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) using B cell-deficient mice (&mgr;MT) and mice bearing the X-linked immunodeficiency (xid).
The mice were immunized with MOG(1-125 )in complete Freund's adjuvant but without use of pertussis toxin.
B cell-deficient &mgr;MT mice on different genetic backgrounds (C57BL/10 and DBA/1 strains) developed EAE, although with a reduced clinical severity.
Histological analyses revealed decreased demyelination in the central nervous system while the influx of inflammatory cells was similar or only slightly reduced as compared to B cell-sufficient control mice.
Xid mice on the DBA/1 background also developed disease with a reduced disease severity.
The anti-MOG antibody response in the xid mice was decreased, while the T cell response to MOG was unaffected.
We thus demonstrate that B cells are not critical for the development of MOG-induced EAE but contribute to the severity.
The contribution of B cells to pathogenesis appears to be mainly through demyelination rather than through inflammation.