Experimental autoimmune encephalomyelitis induction in genetically B cell-deficient mice

被引:539
作者
Wolf, SD [1 ]
Dittel, BN [1 ]
Hardardottir, F [1 ]
Janeway, CA [1 ]
机构
[1] YALE UNIV, SCH MED, HOWARD HUGHES MED INST, IMMUNOBIOL SECT, NEW HAVEN, CT 06510 USA
关键词
D O I
10.1084/jem.184.6.2271
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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 mu chain transmembrane region (B10.PL mu MT). By immunizing B10.PL and B10.PL mu MT 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.PL mu MT 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.
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收藏
页码:2271 / 2278
页数:8
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