CD1-restricted T-cells influence IgG subclass and IgE production

被引:12
作者
Fujieda, S [1 ]
Sieling, PA
Modlin, RL
Saxon, A
机构
[1] Fukui Med Univ, Dept Otorhinolaryngol, Fukui 91011, Japan
[2] Univ Calif Los Angeles, Sch Med, Jonsson Comprehens Canc Ctr Inst, Los Angeles, CA USA
[3] Univ Calif Los Angeles, Sch Med, Inst Mol Biol, Los Angeles, CA USA
[4] Univ Calif Los Angeles, Sch Med, Dept Microbiol & Immunol, Los Angeles, CA USA
[5] Univ Calif Los Angeles, Sch Med, Div Dermatol, Los Angeles, CA USA
[6] Univ Calif Los Angeles, Sch Med, Dept Med, Div Clin Immunol Allergy,Hart & Louise Lyon Lab, Los Angeles, CA USA
关键词
CD1; CD1b; Ige subclass; IgE; isotype switching; IFN-gamma; IL-4;
D O I
10.1016/S0091-6749(98)70362-8
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Background: Human CD1 has recently emerged as a third family of antigen-presenting molecules that is distinct from either major histocompatibility complex class I or class II. Objective: We investigated whether the CD1b-restricted T-cell interaction with antigen alters human IgG subclass and IgE isotype production. Methods: CD1b-restricted antigen-specific T cells derived from the skin lesion of a patient with leprosy were stimulated with their cognate antigen, lipoarabinomman (LAM) of Mycobacterium leprae, in the presence of CD1(+) antigen-presenting cells and tested for their ability to alter IgG subclass and IgE production from IgD(+) B cells. Results: CD1-restricted T cells cultured with CD1(+) antigen-presenting cells in the absence of LAM induced IgG1, IgG3, IgG4, and IgE, whereas CD1b-restricted T cells cultured in the presence of LAM induced IgG1 and IgG3 and inhibited production of IgG4 and IgE. Production of IgG4 and IgE was rescued in the CD1-restricted system by the addition of anti-interferon-gamma. IgG1 production was not induced under any circumstances. Conclusion: In this study we demonstrated that a specific CD1b-restricted T-cell line can behave similarly to classically-restricted T-h1-type T cells. CD1b-restricted T-cells of this type may regulate immune responses to microbial pathogens by simultaneously enhancing cell-mediated immunity and downregulating IgG4 and IgE responses.
引用
收藏
页码:545 / 551
页数:7
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