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Secondary lymphoid organs and CCR7 are dispensable for intestinal Th17 and Foxp3+ Treg cell differentiation
Author(s) -
Geem Duke,
Medina Oscar,
Kim Wooki,
Huang Clifton,
Newberry Rodney,
Denning Timothy Luke
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.136.4
Subject(s) - foxp3 , immunology , adoptive cell transfer , mesenteric lymph nodes , biology , regulatory t cell , immune system , spleen , microbiology and biotechnology , c c chemokine receptor type 7 , lymphatic system , il 2 receptor , t cell , chemokine , chemokine receptor
The intestinal immune system maintains homeostasis by promoting tolerance to the microbiota and food antigens while mounting inflammatory responses towards pathogens. Effector and Foxp3+ Treg cells are enriched in the intestinal lamina propria (LP) and are believed to be generated in the mesenteric lymph nodes (mLN) upon instruction by migrating CCR7+ LP dendritic cells. Herein, we demonstrate using multi‐color flow cytometry normal frequencies and cell numbers of Th17 cells and functional Foxp3+ Treg cells in the intestinal LP of mice deficient in lymphotoxin (LT)α, LTβR, and CCR7. In the absence of secondary lymphoid organs due to LTα deficiency, CD4+ T cell differentiation was not simply shifted to the spleen since splenectomized LTα‐deficient mice exhibited no defects in intestinal Th17 or Foxp3+ Treg cells. Using an OT‐II adoptive transfer system, naïve OT‐II CD4+ T cells differentiated into induced Foxp3+ Treg cells in the intestine in response to the feeding of ovalbumin to LTα‐deficient mice. Collectively, these data suggest that secondary lymphoid organs including mLN are not required for the differentiation of resident intestinal Th17 and Foxp3+ Treg cells and implicate the intestinal LP as a potentially important site for this process. Supported by NIH grants (AA01787001, AI083554), Career Development Award from CCFA, and Emory Egleston Children's Research Center seed grant to T.L.D.