Tolerance Induction of IgG+ Memory B Cells by T Cell-Independent Type II Antigens

被引:17
作者
Haniuda, Kei [1 ]
Nojima, Takuya [1 ]
Ohyama, Kyosuke [1 ]
Kitamura, Daisuke [1 ]
机构
[1] Tokyo Univ Sci, Res Inst Biol Sci, Div Mol Biol, Chiba 2780022, Japan
基金
日本学术振兴会;
关键词
GERMINAL-CENTERS; IN-VIVO; PNEUMOCOCCAL POLYSACCHARIDE; SMALLPOX VACCINATION; IMMUNOLOGICAL MEMORY; AFFINITY MATURATION; IMMUNE-RESPONSES; CUTTING EDGE; RECEPTOR; IMMUNOGLOBULIN;
D O I
10.4049/jimmunol.1100213
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Memory B cells generated during a T cell-dependent immune response rapidly respond to a secondary immunization by producing abundant IgG Abs that bind cognate Ag with high affinity. It is currently unclear whether this heightened recall response by memory B cells is due to augmented IgG-BCR signaling, which has only been demonstrated in the context of naive transgenic B cells. To address this question, we examined whether memory B cells can respond in vivo to Ags that stimulate only through BCR, namely T cell-independent type II (TI-II) Ags. In this study, we show that the TI-II Ag (4-hydroxy-3-nitrophenyl) acetyl (NP)-Ficoll cannot elicit the recall response in mice first immunized with the T cell-dependent Ag NP-chicken gamma-globulin. Moreover, the NP-Ficoll challenge in vivo as well as in vitro significantly inhibits a subsequent recall response to NP-chicken gamma-globulin in a B cell-intrinsic manner. This NP-Ficoll-mediated tolerance is caused by the preferential elimination of IgG(+) memory B cells binding to NP with high affinity. These data indicate that BCR cross-linking with a TI-II Ag does not activate IgG(+) memory B cells, but rather tolerizes them, identifying a terminal checkpoint of memory B cell differentiation that may prevent autoimmunity. The Journal of Immunology, 2011, 186: 5620-5628.
引用
收藏
页码:5620 / 5628
页数:9
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