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From the Howard Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06510

Experimental autoimmune encephalomyelitis (EAE) is an animal model for autoimmune central nervous system disease mediated by CD4 T cells. To examine the role of B cells in the induction of EAE, we used B10.PL (I-A^u) mice rendered deficient in B cells by deletion of their µ chain transmembrane region (B10.PLµMT). By immunizing B10.PL and B10.PLµMT mice with the NH-terminal myelin basic protein encephalitogenic peptide Ac1-11, we observed no difference in the onset or severity of disease in the absence of mature B cells. There was, however, a greater variation in disease onset, severity, and especially of recovery in the B cell–deficient mice compared to controls. B10.PLµMT mice rarely returned to normal in the absence of B cells. Taken together, our data suggest that B cells do not play a role in the activation of encephalitogenic T cells, but may contribute to the immune modulation of acute EAE. The mechanisms to explain these effects are discussed.

Dr. Charles A. Janeway Jr., Howard Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06510.

¹ Abbreviations used in this paper: CNS, central nervous system; DC, dendritic cell; EAE, experimental autoimmune encephalomyelitis; HPRT, hypoxanthine-guanine phosphoribosyl transferase; MBP, myelin basic protein; RT, reverse transcriptase.

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