Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 38, Issue 12, Pages 3411-3425Publisher
WILEY
DOI: 10.1002/eji.200838432
Keywords
Animal models; B-cell development; CD8 T cells; Enteric microbiota
Categories
Funding
- NIH [P30 DK349870, P40 RR018603, DK46763, DK69434, AI52031, HD37091, CA016042]
- Crohn's and Colitis Foundation of America
- Broad Medical Research Foundation
- Elizabeth Campbell Endowment
- McDonnell Scholar Award
- Leukemia and Lymphoma Society Scholar Award,
- Joan J. Drake Grant for Excellence in Cancer Research
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R01HD037091] Funding Source: NIH RePORTER
- NATIONAL CANCER INSTITUTE [P30CA016042] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [P40RR018603] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [T32AI052031] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK069434, P01DK046763] Funding Source: NIH RePORTER
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Since enteric microbial composition is a distinctive and stable individual trait, microbial heterogeneity may confer lifelong, non-genetic differences between individuals. Here we report that C57BL/6 mice bearing restricted flora microbiota, a distinct but diverse resident enteric microbial community, are numerically and functionally deficient in marginal zone (MZ) B cells. Surprisingly, MZ B-cell levels are minimally affected by germ-free conditions or null mutations of various TLR signaling molecules. In contrast, MZ B-cell depletion is exquisitely dependent on cytolytic CDS+ T cells, and includes targeting of a cross-reactive microbial/endogenous MHC class 1B antigen. Thus, members of certain enteric microbial communities link with CD8(+) T cells as a previously unappreciated mechanism that shapes innate immunity dependent on innate-like B cells.
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