title: Involvement of CD161+ Vδ1+ γδ T cells in systemic sclerosis: association with interstitial pneumonia.
abstract: OBJECTIVE
  Interstitial pneumonia (IP) is a chronic progressive interstitial lung disease associated with high mortality and poor prognosis. However, the pathogenesis of IP remains to be elucidated. The aim of this study was to clarify the role of CD161(+) Vδ1(+) γδ T cells in SSc patients with IP.
  
  
  METHODS
  The proportion of CD161(+) Vδ1(+) γδ T cells in peripheral blood mononuclear cells (PBMCs) and serum sialylated carbohydrate antigen (KL-6) levels were determined. GeneChip analysis was performed with CD161(-) and CD161(+) Vδ1(+) γδ T cells. Cytokine and chemokine expression from CD161(+) Vδ1(+) γδ T cells was measured and used to evaluate the effect of culture supernatant on fibroblast proliferation.
  
  
  RESULTS
  The proportion of CD161(+) Vδ1(+) γδ T cells was significantly higher in SSc than healthy controls (HCs) and correlated negatively with serum KL-6 levels in IP-positive SSc patients. The gene and mRNA expression level of chemokine ligand 3 (CCL3) was markedly higher in CD161(+) Vδ1(+) γδ T cells than in CD161(-) Vδ1(+) γδ T cells. CD161(+) Vδ1(+) γδ T cells in IP-positive SSc patients showed higher production of CCL3 and lower production of IFN-γ than in HCs. Culture supernatant derived from IP-negative and IP-positive SSc patients promoted fibroblast proliferation, whereas that from HCs did not.
  
  
  CONCLUSIONS
  The small proportion and the altered cell functions of CD161(+) Vδ1(+) γδ T cells among PBMCs in SSc patients play a role in the pathogenesis of IP. These findings suggest that CD161(+) Vδ1(+) γδ T cells may play a regulatory role in the pathogenesis of IP in SSc patients via IFN-γ production.
authors: Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
authors: Seiji
authors: S
authors: Segawa
authors: Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
authors: Daisuke
authors: D
authors: Goto
authors: Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
authors: Masanobu
authors: M
authors: Horikoshi
authors: Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
authors: Yuya
authors: Y
authors: Kondo
authors: Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
authors: Naoto
authors: N
authors: Umeda
authors: Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
authors: Shinnya
authors: S
authors: Hagiwara
authors: Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
authors: Masahiro
authors: M
authors: Yokosawa
authors: Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
authors: Tomoya
authors: T
authors: Hirota
authors: Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
authors: Haruka
authors: H
authors: Miki
authors: Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
authors: Hiroto
authors: H
authors: Tsuboi
authors: Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
authors: Hiroshi
authors: H
authors: Ogishima
authors: Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
authors: Takeshi
authors: T
authors: Suzuki
authors: Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
authors: Isao
authors: I
authors: Matsumoto
authors: Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan. tsumida@md.tsukuba.ac.jp.
authors: Takayuki
authors: T
authors: Sumida
mesh_terms: D000328:Adult; D000368:Aged; D049109:Cell Proliferation; D002478:Cells, Cultured; D054405:Chemokine CCL3 / Q000276:immunology / Q000378:metabolism; D054407:Chemokine CCL4 / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D005260:Female; D005347:Fibroblasts / Q000276:immunology; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis / Q000276:immunology; D017563:Lung Diseases, Interstitial / Q000209:etiology / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D055651:NK Cell Lectin-Like Receptor Subfamily B / Q000097:blood*; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000097:blood*; D012595:Scleroderma, Systemic / Q000150:complications / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology
chemical_list: C515429:CCL3 protein, human; C066507:CCL4 protein, human; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D016207:Cytokines; C527203:KLRB1 protein, human; D055651:NK Cell Lectin-Like Receptor Subfamily B; D016692:Receptors, Antigen, T-Cell, gamma-delta; D007371:Interferon-gamma
keywords: CCL3; CD161; KL-6; gamma-delta T cell; interferon-γ, natural killer receptors; interstitial pneumonia; systemic sclerosis