Control of Toll-like Receptor-mediated T Cell-independent Type 1 Antibody Responses by the Inducible Nuclear Protein IκB-ζ

被引:17
作者
Hanihara-Tatsuzawa, Fumito [1 ]
Miura, Hanae [1 ]
Kobayashi, Shuhei [1 ]
Isagawa, Takayuki [2 ]
Okuma, Atsushi [1 ]
Manabe, Ichiro [3 ]
MaruYama, Takashi [1 ,4 ]
机构
[1] Tohoku Univ, Grad Sch Life Sci, Dept Dev Biol & Neurosci, Lab Cell Recognit & Response, Sendai, Miyagi 9808578, Japan
[2] Tokyo Med & Dent Univ, Med Res Inst, Dept Genom Pathol, Tokyo 1138510, Japan
[3] Univ Tokyo, Grad Sch Med, Dept Cardiovasc Med, Tokyo 38655, Japan
[4] Gifu Univ, Sch Med, Lab Cell Signaling, Gifu 5011194, Japan
基金
日本学术振兴会;
关键词
CLASS-SWITCH RECOMBINATION; HUMORAL IMMUNE-RESPONSE; VIVO CD40-GP39 INTERACTIONS; CYTIDINE DEAMINASE AID; STREPTOCOCCUS-PNEUMONIAE; DNA RECOMBINATION; MESSENGER-RNA; GENE-EXPRESSION; ACTIVATION; TRANSCRIPTION;
D O I
10.1074/jbc.M114.553230
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Antibody responses have been classified as being either T cell-dependent or T cell-independent (TI). TI antibody responses are further classified as being either type 1 (TI-1) or type 2 (TI-2), depending on their requirement for B cell-mediated antigen receptor signaling. Although the mechanistic basis of antibody responses has been studied extensively, it remains unclear whether different antibody responses share similarities in their transcriptional regulation. Here, we show that mice deficient in I kappa B-zeta, specifically in their B cells, have impaired TI-1 antibody responses but normal T cell-dependent and TI-2 antibody responses. The absence of I kappa B-zeta in B cells also impaired proliferation triggered by Toll-like receptor (TLR) activation, plasma cell differentiation, and class switch recombination (CSR). Mechanistically, I kappa B-zeta-deficient B cells could not induce TLR-mediated induction of activation-induced cytidine deaminase (AID), a class-switch DNA recombinase. Retroviral transduction of AID in I kappa B-zeta-deficient B cells restored CSR activity. Furthermore, acetylation of histone H3 in the vicinity of the transcription start site of the gene that encodes AID was reduced in I kappa B-zeta-deficient B cells relative to I kappa B-zeta-expressing B cells. These results indicate that I kappa B-zeta regulates TLR-mediated CSR by inducing AID. Moreover, I kappa B-zeta defines differences in the transcriptional regulation of different antibody responses.
引用
收藏
页码:30925 / 30936
页数:12
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