Almost all mice lacking specific molecules associated with regulatory T cells or barrier function develop intestinal inflammation in the colon, but not in the small intestine (SI). Therefore, intestinal homeostasis of the SI may be tightly controlled by other mechanisms. To determine the role of CCR9+ plasmacytoid dendritic cells (pDCs) in intestinal homeostasis of the SI we transferred CD4+CD45RBhigh T cells into ccr9-/-×rag-2-/- mice. We showed that CCL25, a counterpart chemokine for CCR9, is constitutively expressed in the SI but not the colon and spleen of rag-2-/- or ccr9-/-×rag-2-/- mice before or after transfer of CD4+CD45RBhigh T cells. The ccr9-/-×rag-2-/- mice did not develop spontaneous intestinal inflammation in the SI and colon. Mice of both genotype where CD4+CD45RBhigh T cells were transferred developed colitis. However, the ccr9-/-×rag-2-/- mice also developed ileitis with marked infiltration of Th1 cells. These results suggest that CCR9+ pDCs are possibly small, regulatory, antigen-presenting cells of the intestine that suppress intestinal inflammation.
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