title: Differing distributions of CXCR3- and CCR4-positive cells among types of interstitial pneumonia associated with collagen vascular diseases.
abstract: Interstitial pneumonia (IP) is an important complication in collagen vascular diseases (CVDs). We examined the distribution of helper T cell subsets in lung biopsies of cases of IP associated with CVD (CVD-IP). The tissues from 27 CVD-IP patients with rheumatoid arthritis (RA), 8 with polymyositis or dermatomyositis (PM/DM), and 8 with systemic sclerosis (SSc) were compared with those from 10 patients with idiopathic pulmonary fibrosis (IPF) in our previous study. The expressions of CXCR3 and CCR4 (chemokine receptors associated in vitro with Th1 and Th2 cells, respectively) in the mononuclear infiltrate were analyzed immunohistochemically. The positive cells were semiquantified in fibrosing areas of the CVD-IP and IPF cases. The number of CXCR3-positive cells was significantly greater in RA-IP than in PM/DM-IP, SSc-IP, or IPF, whereas there were fewer CCR4-positive cells in RA-IP, PM/DM-IP, and SSc-IP than in IPF. The CXCR3-/CCR4-positive cells ratio was significantly higher in RA-IP and PM/DM-IP (but not in SSc-IP) than in IPF. These results support previous reports of the dominance of Th2 cells in some SSc-IP and IPF cases. However, Th1-type immune responses may predominate in RA-IP and PM/DM-IP. Our findings suggest that the pathogenesis of CVD-IPs differs with the helper T cell subset.
authors.affiliation: Department of Internal Medicine and Molecular Science, Nagoya City University Medical School, Kawasumi 1, Mizyho-ku, Nagoya, Aichi, 467-8601, Japan.
authors.forename: Shigeki
authors.initials: S
authors.lastname: Shimizu
authors.forename: Takeo
authors.initials: T
authors.lastname: Yoshinouchi
authors.forename: Takashi
authors.initials: T
authors.lastname: Niimi
authors.forename: Yuji
authors.initials: Y
authors.lastname: Ohtsuki
authors.forename: Jiro
authors.initials: J
authors.lastname: Fujita
authors.forename: Hiroyoshi
authors.initials: H
authors.lastname: Maeda
authors.forename: Shigeki
authors.initials: S
authors.lastname: Sato
authors.forename: Ichiro
authors.initials: I
authors.lastname: Yamadori
authors.forename: Tadaaki
authors.initials: T
authors.lastname: Eimoto
authors.forename: Ryuzo
authors.initials: R
authors.lastname: Ueda
mesh_terms: D000328:Adult; D000368:Aged; D018951:Antigens, CD20 / Q000032:analysis; D001172:Arthritis, Rheumatoid / Q000276:immunology; D003240:Connective Tissue Diseases / Q000276:immunology*; D005260:Female; D006801:Humans; D017563:Lung Diseases, Interstitial / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D011658:Pulmonary Fibrosis / Q000276:immunology; D054398:Receptors, CCR4; D054367:Receptors, CXCR3; D019707:Receptors, Chemokine / Q000032:analysis*; D012595:Scleroderma, Systemic / Q000276:immunology; D012859:Sjogren's Syndrome / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology; D014652:Vascular Diseases / Q000276:immunology*
chemical_list: D018951:Antigens, CD20; C515354:CCR4 protein, human; C515187:CXCR3 protein, human; D054398:Receptors, CCR4; D054367:Receptors, CXCR3; D019707:Receptors, Chemokine