Intestinal bacteria induce TSLP to promote mutualistic T-cell responses
I Mosconi, MB Geuking, MM Zaiss, JC Massacand… - Mucosal …, 2013 - nature.com
I Mosconi, MB Geuking, MM Zaiss, JC Massacand, C Aschwanden, CKC Kwong Chung…
Mucosal immunology, 2013•nature.comThymic stromal lymphopoietin (TSLP) is constitutively expressed in the intestine and is
known to regulate inflammation in models of colitis. We show that steady-state TSLP
expression requires intestinal bacteria and has an important role in limiting the expansion of
colonic T helper type 17 (Th17) cells. Inappropriate expansion of the colonic Th17 cells
occurred in response to an entirely benign intestinal microbiota, as determined following the
colonization of germ-free C57BL/6 or TSLPR−/− mice with the altered Schaedler flora (ASF) …
known to regulate inflammation in models of colitis. We show that steady-state TSLP
expression requires intestinal bacteria and has an important role in limiting the expansion of
colonic T helper type 17 (Th17) cells. Inappropriate expansion of the colonic Th17 cells
occurred in response to an entirely benign intestinal microbiota, as determined following the
colonization of germ-free C57BL/6 or TSLPR−/− mice with the altered Schaedler flora (ASF) …
Abstract
Thymic stromal lymphopoietin (TSLP) is constitutively expressed in the intestine and is known to regulate inflammation in models of colitis. We show that steady-state TSLP expression requires intestinal bacteria and has an important role in limiting the expansion of colonic T helper type 17 (Th17) cells. Inappropriate expansion of the colonic Th17 cells occurred in response to an entirely benign intestinal microbiota, as determined following the colonization of germ-free C57BL/6 or TSLPR−/− mice with the altered Schaedler flora (ASF). TSLP–TSLPR (TSLP receptor) interactions also promoted the expansion of colonic Helios− Foxp3+ regulatory T cells, necessary for the control of inappropriate Th17 responses following ASF bacterial colonization. In summary, these data reveal an important role for TSLP-TSLPR signaling in promoting steady-state mutualistic T-cell responses following intestinal bacterial colonization.
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