title: The differential role of L-selectin and ICAM-1 in Th1-type and Th2-type contact hypersensitivity.
abstract: Sensitization and challenge using DNFB induce contact hypersensitivity (CHS) with predominant type 1 helper (Th1) cell infiltration, whereas those using FITC generate CHS with Th2 cell infiltration. CHS results from inflammatory cell infiltration, a process that is highly regulated by the expression of multiple adhesion molecules. We attempted to determine the role of L-selectin and ICAM-1 in Th1- and Th2-type CHS induced by DNFB or FITC in mice lacking either L-selectin, ICAM-1, or both. Th1-type CHS induced by DNFB was inhibited by L-selectin and/or ICAM-1 deficiency, which was associated with reduced IFN-gamma expression. Similarly, Th2-type CHS induced by FITC was inhibited by L-selectin deficiency. However, Th2-type CHS was increased by ICAM-1 deficiency and accompanied by increased Th2 cytokine expression. Infiltration of in vitro-generated Th1 cells into the FITC-challenged skin decreased in ICAM-1-deficient mice, whereas in vitro-generated Th2 cell infiltration increased, suggesting that ICAM-1 mediates Th1 cell migration and that in the absence of ICAM-1, Th1 cell recruitment decreased, whereas relative Th2 cell migration increased. These results suggest that ICAM-1 mediates Th1 cell recruitment irrespective of DNFB or FITC and that L-selectin recruits Th1 cells in Th1-type CHS, whereas it recruits Th2 cells in Th2-type CHS.
authors.affiliation: Department of Dermatology, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki, Japan.
authors.forename: Asako
authors.initials: A
authors.lastname: Ogawa
authors.forename: Ayumi
authors.initials: A
authors.lastname: Yoshizaki
authors.forename: Koichi
authors.initials: K
authors.lastname: Yanaba
authors.forename: Fumihide
authors.initials: F
authors.lastname: Ogawa
authors.forename: Toshihide
authors.initials: T
authors.lastname: Hara
authors.forename: Eiji
authors.initials: E
authors.lastname: Muroi
authors.forename: Motoi
authors.initials: M
authors.lastname: Takenaka
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Shimizu
authors.forename: Minoru
authors.initials: M
authors.lastname: Hasegawa
authors.forename: Manabu
authors.initials: M
authors.lastname: Fujimoto
authors.forename: Thomas F
authors.initials: TF
authors.lastname: Tedder
authors.forename: Shinichi
authors.initials: S
authors.lastname: Sato
mesh_terms: D000818:Animals; D000888:Antibodies, Anti-Idiotypic / Q000494:pharmacology; D002465:Cell Movement / Q000502:physiology; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism; D003877:Dermatitis, Contact / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D004139:Dinitrofluorobenzene / Q000009:adverse effects; D004195:Disease Models, Animal; D016650:Fluorescein-5-isothiocyanate / Q000009:adverse effects; D006241:Haptens / Q000494:pharmacology; D007073:Immunoglobulin E / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000276:immunology / Q000502:physiology*; D007371:Interferon-gamma / Q000378:metabolism; D019041:L-Selectin / Q000235:genetics / Q000276:immunology / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D018417:Th1 Cells / Q000473:pathology / Q000502:physiology*; D018418:Th2 Cells / Q000473:pathology / Q000502:physiology*
chemical_list: D000888:Antibodies, Anti-Idiotypic; D016207:Cytokines; D006241:Haptens; D018799:Intercellular Adhesion Molecule-1; D019041:L-Selectin; D007073:Immunoglobulin E; D007371:Interferon-gamma; D004139:Dinitrofluorobenzene; D016650:Fluorescein-5-isothiocyanate