Maternal IgG and IgA Antibodies Dampen Mucosal T Helper Cell Responses in Early Life

被引:211
作者
Koch, Meghan A. [1 ]
Reiner, Gabrielle L. [1 ,2 ]
Lugo, Kyler A. [1 ,3 ]
Kreuk, Lieselotte S. M. [1 ]
Stanbery, Alison G. [1 ]
Ansaldo, Eduard [1 ]
Seher, Thaddeus D. [1 ,4 ]
Ludington, William B. [1 ]
Barton, Gregory M. [1 ]
机构
[1] Univ Calif Berkeley, Dept Mol & Cell Biol, Div Immunol & Pathogenesis, 229 Stanley Hall, Berkeley, CA 94720 USA
[2] Aduro Biotech Inc, Berkeley, CA 94710 USA
[3] Stanford Univ, Stanford Sch Med, Dept Microbiol & Immunol, Stanford, CA 94305 USA
[4] Univ Calif Merced, Dept Quantitat & Syst Biol, Merced, CA 95343 USA
关键词
GUT MICROBIOTA; PLASMA-CELLS; BACTERIA; INNATE; IMMUNITY; IMMUNOGLOBULINS; INDUCTION; HOMEOSTASIS; GENERATION; INFECTION;
D O I
10.1016/j.cell.2016.04.055
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
To maintain a symbiotic relationship between the host and its resident intestinal microbiota, appropriate mucosal T cell responses to commensal antigens must be established. Mice acquire both IgG and IgA maternally; the former has primarily been implicated in passive immunity to pathogens while the latter mediates host-commensal mutualism. Here, we report the surprising observation that mice generate T cell-independent and largely Toll-like receptor (TLR)-dependent IgG2b and IgG3 antibody responses against their gut microbiota. We demonstrate that maternal acquisition of these antibodies dampens mucosal T follicular helper responses and subsequent germinal center B cell responses following birth. This work reveals a feedback loop whereby T cell-independent, TLR-dependent antibodies limit mucosal adaptive immune responses to newly acquired commensal antigens and uncovers a broader function for maternal IgG.
引用
收藏
页码:827 / 841
页数:15
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