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The control of inflammatory diseases requires functional regulatory T cells (Tregs) with significant Gata-3 expression. Here we address the inhibitory role of Tregs on intestinal tumorigenesis in the  Apc   /Min+  mouse model that resembles human familial adenomatous polyposis (FAP).  Apc   /Min+  mice had a markedly increased frequency of Foxp3+ Tregs and yet decreased Gata-3 expression in the lamina propria. To address the role of heterozygous  Apc  gene mutation in Tregs, we generated  Foxp3-Cre ,  Apc   flox/+  mice. Tregs from these mice effectively inhibited tumorigenesis comparable to wild type Tregs after adoptive transfer into  Apc   /Min+  mice, demonstrating that the heterozygous  Apc  gene mutation in Tregs does not induce the loss of control over tumor microenvironment. Adoptive transfer of in vitro generated  Apc   /Min+  iTregs (inducible Tregs) failed to inhibit intestinal tumorigenesis, suggesting that naïve CD4 T cells generated from  Apc   /Min+  mice thymus were impaired. We also showed that adoptively transferred IL-17A-deficient  Apc   /Min+  Tregs inhibited tumor growth, suggesting that IL-17A was critical to impair the tumor regression function of  Apc   /Min+  Tregs. Taken together, our results suggest that both T cell development in a functional thymus and IL-17A control the ability of Treg to inhibit intestinal tumorigenesis in  Apc   /Min+  mice.

journal of immunology research

Spontaneous Intestinal Tumorigenesis in<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:msup><mml:mrow><mml:mi>A</mml:mi><mml:mi>p</mml:mi><mml:mi>c</mml:mi></mml:mrow><mml:mrow><mml:mo>/</mml:mo><mml:mi mathvariant="normal">M</mml:mi><mml:mi mathvariant="normal">i</mml:mi><mml:mi mathvariant="normal">n</mml:mi><mml:mo>+</mml:mo></mml:mrow></mml:msup></mml:mrow></mml:math>Mice Requires Altered T Cell Development with IL-17A

Spontaneous Intestinal Tumorigenesis inApc/Min+Mice Requires Altered T Cell Development with IL-17A