Impaired development of Th2 cells in IL-13-deficient mice

被引:320
作者
McKenzie, GJ
Emson, CL
Bell, SE
Anderson, S
Fallon, P
Zurawski, G
Murray, R
Grencis, R
McKenzie, ANJ
机构
[1] MRC, Mol Biol Lab, Cambridge CB2 2QH, England
[2] Univ Cambridge, Wellcome Trust Immunol Unit, Cambridge CB2 2SP, England
[3] DNAX Res Inst Mol & Cellular Biol Inc, Palo Alto, CA 94304 USA
[4] Univ Cambridge, Dept Pathol, Cambridge CB2 1QP, England
[5] Univ Manchester, Sch Biol Sci, Manchester M13 9PT, Lancs, England
基金
英国惠康基金;
关键词
D O I
10.1016/S1074-7613(00)80625-1
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We report that Th2 cell cultures generated using T cells or splenocytes from IL-13-deficient mice produce significantly reduced levels of IL-4, IL-5, and IL-10 compared with wild-type. In contrast, IL-4 and IL-5 production by mast cells stimulated in vitro with PMA, ionomycin, or IgE cross-linking are unaffected. In vitro Th2 cell differentiation cannot be rescued by the addition of exogenous factors, but in vivo antigen challenge and administration of IL-13 can increase Th2-like cytokine responses as can infection with the parasitic nematode Nippostrongylus brasiliensis. IL-13-deficient mice also have lower basal levels of serum IgE and biased antigen-specific immunoglobulin responses. Thus, IL-13 is an important regulator of Th2 commitment and may therefore play a central role in atopy and infectious diseases.
引用
收藏
页码:423 / 432
页数:10
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