title: Pertussis toxin-sensitive signal controls the trafficking of thymocytes across the corticomedullary junction in the thymus.
abstract: We investigated a role of chemokines in thymocyte trafficking. Genes encoding stromal cell-derived factor-1 and its receptor CXCR4 were detected in the cortex by in situ hybridization. Early immigrant cells did not express CXCR4, whereas their descendant CD44+CD25+CD4-CD8- cells did. CXCR4 expression was down-modulated when CD4+CD8+ double-positive cells became CD4+CD8- or CD4-CD8+ single-positive (SP) cells. Positively selected CD69+CD3intermediate cells gained CCR4, of which ligand, thymus activation-regulated chemokine, was expressed in the medulla. At the next developmental stage, CD69-CD3high cells lost CCR4 but gained CCR7. These results suggest that thymocytes use different chemokines along with their development. Blockade of chemokine receptor-mediated signaling by pertussis toxin perturbed the normal distribution of SP cells and resulted in the accumulation of SP cells in the cortex. Thus, a pertussis toxin-sensitive event controls the trafficking of SP cells across the corticomedullary junction.
authors.affiliation: Divisions of Radiation, The Fifth Research Group, National Institute of Radiological Sciences, Chiba, Japan. gsuzuki@nirs.go.jp
authors.forename: G
authors.initials: G
authors.lastname: Suzuki
authors.forename: H
authors.initials: H
authors.lastname: Sawa
authors.forename: Y
authors.initials: Y
authors.lastname: Kobayashi
authors.forename: Y
authors.initials: Y
authors.lastname: Nakata
authors.forename: K i
authors.initials: Ki
authors.lastname: Nakagawa
authors.forename: A
authors.initials: A
authors.lastname: Uzawa
authors.forename: H
authors.initials: H
authors.lastname: Sakiyama
authors.forename: S
authors.initials: S
authors.lastname: Kakinuma
authors.forename: K
authors.initials: K
authors.lastname: Iwabuchi
authors.forename: K
authors.initials: K
authors.lastname: Nagashima
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000302:isolation & purification; D000945:Antigens, Differentiation, T-Lymphocyte / Q000302:isolation & purification; D017252:CD3 Complex / Q000302:isolation & purification; D054377:Chemokine CXCL12; D019743:Chemokines, CXC / Q000235:genetics / Q000302:isolation & purification*; D002634:Chemotaxis, Leukocyte / Q000187:drug effects*; D002678:Chimera; D017403:In Situ Hybridization; D037181:Lectins, C-Type; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D037342:Pertussis Toxin; D012333:RNA, Messenger / Q000302:isolation & purification; D054398:Receptors, CCR4; D054400:Receptors, CCR7; D019718:Receptors, CXCR4 / Q000235:genetics / Q000302:isolation & purification*; D019707:Receptors, Chemokine / Q000302:isolation & purification; D015398:Signal Transduction; D013950:Thymus Gland / Q000166:cytology / Q000187:drug effects / Q000276:immunology*; D014018:Tissue Distribution; D010566:Virulence Factors, Bordetella / Q000494:pharmacology*; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D017252:CD3 Complex; D054377:Chemokine CXCL12; D019743:Chemokines, CXC; D037181:Lectins, C-Type; D037342:Pertussis Toxin; D012333:RNA, Messenger; D054398:Receptors, CCR4; D054400:Receptors, CCR7; D019718:Receptors, CXCR4; D019707:Receptors, Chemokine; D010566:Virulence Factors, Bordetella; D000099192:CD69 Antigens; C515355:Ccr4 protein, mouse; C515371:Ccr7 protein, mouse; C515256:Cxcl12 protein, mouse