Notch2-dependent classical dendritic cells orchestrate intestinal immunity to attaching-and-effacing bacterial pathogens

作者：Satpathy Ansuman T; Briseno Carlos G; Lee Jacob S; Ng Dennis; Manieri Nicholas A; Wumesh K C; Wu Xiaodi; Thomas Stephanie R; Lee Wan Ling; Turkoz Mustafa; McDonald Keely G; Meredith Matthew M; Song Christina; Guidos Cynthia J; Newberry Rodney D; Ouyang Wenjun; Murphy Theresa L; Stappenbeck Thaddeus S; Gommerman Jennifer L; Nussenzweig Michel C; Colonna Marco; Kopan Raphael; Murphy Kenneth M^*

来源：Nature Immunology, 2013, 14(9): 937-+.

DOI：10.1038/ni.2679

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.

• 出版日期2013-9