OX40-deficient mice are defective in Th cell proliferation but are competent in generating B cell and CTL responses after virus infection

被引:262
作者
Kopf, M
Ruedl, C
Schmitz, N
Gallimore, A
Lefrang, K
Ecabert, B
Odermatt, B
Bachmann, MF
机构
[1] Basel Inst Immunol, CH-4005 Basel, Switzerland
[2] Univ Zurich, Dept Pathol, CH-8091 Zurich, Switzerland
[3] John Radcliffe Hosp, Inst Mol Med, Oxford OX3 9DS, England
关键词
D O I
10.1016/S1074-7613(00)80144-2
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
OX40, a member of the TNF receptor superfamily, is expressed on activated T cells and implicated in stimulation of T cells and T-dependent humoral responses. We generated OX40(-/-) mice and found that the formation of extrafollicular plasma cells, germinal centers, and antibody responses was independent of OX40. After infection with LCMV and influenza virus, OX40(-/-) mice retain primary and memory cytotoxic T cell responses with normal expansion and decline of specific CTL. In contrast, CD4(+) T cell proliferation and the number of IFN-gamma-producing CD4(+) T cells were reduced in OX40(-/-) mice. Moreover, the number of CD4(+) T cells infiltrating the lungs of influenza virus-infected OX40(-/-) mice was reduced. These results define a unique role of OX40 in the generation of optimal CD4(+) T cell responses in vivo.
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收藏
页码:699 / 708
页数:10
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