Restricted microbiota and absence of cognate TCR antigen leads to an unbalanced generation of Th17 cells.

Lymphoid Tissue Development Unit, Department of Immunology, Institut Pasteur, 75724 Paris, France.
The Journal of Immunology (Impact Factor: 5.36). 02/2011; 186(3):1531-7. DOI: 10.4049/jimmunol.1001723
Source: PubMed

ABSTRACT Retinoic acid-related orphan receptor (ROR)γt(+) TCRαβ(+) cells expressing IL-17, termed Th17 cells, are most abundant in the intestinal lamina propria. Symbiotic microbiota are required for the generation of Th17 cells, but the requirement for microbiota-derived Ag is not documented. In this study, we show that normal numbers of Th17 cells develop in the intestine of mice that express a single TCR in the absence of cognate Ag, whereas the microbiota remains essential for their development. However, such mice, or mice monocolonized with the Th17-inducing segmented filamentous bacteria, fail to induce normal numbers of Foxp3(+) RORγt(+) T cells, the regulatory counterpart of IL-17(+)RORγt(+) T cells. These results demonstrate that a complex microbiota and cognate Ag are required to generate a properly regulated set of RORγt(+) T cells and Th17 cells.

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Available from: Matthias Lochner, Mar 31, 2014
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