title: CCR9+ plasmacytoid dendritic cells in the small intestine suppress development of intestinal inflammation in mice.
abstract: 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(+)CD45RB(high) 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(+)CD45RB(high) T cells. The ccr9(-/-)×rag-2(-/-) mice did not develop spontaneous intestinal inflammation in the SI and colon. Mice of both genotype where CD4(+)CD45RB(high) 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.
authors.affiliation: Department of Gastroenterology and Hepatology, Keio University School of Medicine, Tokyo 160-8582, Japan.
authors.forename: Shinta
authors.initials: S
authors.lastname: Mizuno
authors.forename: Takanori
authors.initials: T
authors.lastname: Kanai
authors.forename: Yohei
authors.initials: Y
authors.lastname: Mikami
authors.forename: Tomohisa
authors.initials: T
authors.lastname: Sujino
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Ono
authors.forename: Atsushi
authors.initials: A
authors.lastname: Hayashi
authors.forename: Tango
authors.initials: T
authors.lastname: Handa
authors.forename: Atsuhiro
authors.initials: A
authors.lastname: Matsumoto
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Nakamoto
authors.forename: Katsuyoshi
authors.initials: K
authors.lastname: Matsuoka
authors.forename: Tadakazu
authors.initials: T
authors.lastname: Hisamatsu
authors.forename: Hiromasa
authors.initials: H
authors.lastname: Takaishi
authors.forename: Toshifumi
authors.initials: T
authors.lastname: Hibi
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D015703:Antigens, CD / Q000235:genetics / Q000276:immunology; D002465:Cell Movement; D019742:Chemokines, CC / Q000235:genetics / Q000276:immunology; D003092:Colitis / Q000150:complications / Q000235:genetics / Q000276:immunology / Q000473:pathology; D003106:Colon / Q000276:immunology / Q000473:pathology; D003433:Crosses, Genetic; D004268:DNA-Binding Proteins / Q000172:deficiency / Q000235:genetics / Q000276:immunology*; D003713:Dendritic Cells / Q000276:immunology* / Q000473:pathology; D007079:Ileitis / Q000150:complications / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D007249:Inflammation / Q000150:complications / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D007421:Intestine, Small / Q000276:immunology* / Q000473:pathology; D051379:Mice; D009928:Organ Specificity; D054388:Receptors, CCR / Q000172:deficiency / Q000235:genetics / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology / Q000473:pathology
chemical_list: D015703:Antigens, CD; C119309:CC chemokine receptor 9; C491541:Ccl25 protein, mouse; D019742:Chemokines, CC; D004268:DNA-Binding Proteins; C499308:Rag2 protein, mouse; D054388:Receptors, CCR