B cell-deficient mice do not develop type II collagen-induced arthritis (CIA)

被引:1
|
作者
Svensson, L [1 ]
Jirholt, J [1 ]
Holmdahl, R [1 ]
Jansson, L [1 ]
机构
[1] Univ Lund, Sect Med Inflammat Res, CMB, S-22100 Lund, Sweden
来源
CLINICAL AND EXPERIMENTAL IMMUNOLOGY | 1998年 / 111卷 / 03期
关键词
B cells; collagen-induced arthritis; autoimmunity; type II collagen;
D O I
暂无
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
To investigate the role of B cells in the development of CIA, a model for rheumatoid arthritis, we investigated susceptibility to CIA in mice lacking B cells due to the deletion of the IgM heavy chain gene (mu MT). The mu MT deletion was backcrossed into two different CIA-susceptible strains, B10.Q and B 10.RIII. Two different variants of the CIA model are inducible in these strains: in B10.Q with rat type II collagen (CII) and in BI0.RIII with bovine CII. Homozygous deletion of the ISM gene led to the absence of B cells and dramatically reduced immunoglobulin levels compared with wild-type mice. The deletion of IgM totally abrogated development of CIA in both strains, although the anti-CII T cell response did not differ between the mu MT and wild-type controls. We conclude that B cells play a crucial role in the development of CIA.
引用
收藏
页码:521 / 526
页数:6
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