期刊
NATURE IMMUNOLOGY
卷 14, 期 9, 页码 937-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2679
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资金
- Howard Hughes Medical Institute
- US National Institutes of Health [AI076427-02, R01 GM55479, R01 DE021255-01, U01 AI095542-01, R01 DK071619, R01 DK064798]
- US Department of Defense [W81XWH-09-1-0185]
- American Heart Association [12PRE8610005, 12PRE12050419]
- Canadian Institutes of Health Research [MOP 67157, FRN 11530]
- National Cancer Institute [P30 CA91842]
Defense against attaching-and-effacing bacteria requires the sequential generation of interleukin 23 (IL-23) and IL-22 to induce protective mucosal responses. Although CD4(+) and NKp46(+) innate lymphoid cells (ILCs) are the critical source of IL-22 during infection, the precise source of IL-23 is unclear. We used genetic techniques to deplete mice of specific subsets of classical dendritic cells (cDCs) and analyzed immunity to the attaching-and-effacing pathogen Citrobacter rodentium. We found that the signaling receptor Notch2 controlled the terminal stage of cDC differentiation. Notch2-dependent intestinal CD11b(+) cDCs were an obligate source of IL-23 required for survival after infection with C. rodentium, but CD103(+) cDCs dependent on the transcription factor Batf3 were not. Our results demonstrate a nonredundant function for CD11b(+) cDCs in the response to pathogens in vivo.
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