title: Increased B7-H1 expression on peripheral blood T cells in oral lichen planus correlated with disease severity.
abstract: BACKGROUND
  Oral lichen planus (OLP) is a chronic and T cell-mediated autoimmune disease whose immunopathogenesis may involve antigen-presentation, T cells activation and migration as well as keratinocytes apoptosis. PD-1/B7-H1 pathway may have a unique function in regulating self-reactive T cells associated with inflammatory response and maintaining tolerance in peripheral tissues. In this study, we aimed to explore the contribution of PD-1/B7-H1 pathway to OLP.
  
  
  METHODS
  We determined the expression of PD-1 and B7-H1 on peripheral blood T cells from OLP cases and analyzed their association with disease severity assessed by RAE (reticular, atrophic and erosive lesion) scoring system. In addition, interferon-γ, interleukin (IL)-2, IL-4, IL-10 and soluble PD-1 concentrations in serum were measured using ELISA. Then, we explored the regulation of PD-1/B7-H1 pathway on T cells immune response in OLP by blockade of PD-1 or B7-H1.
  
  
  RESULTS
  We found that PD-1 and B7-H1 were up-regulated on peripheral blood T cells from OLP patients and B7-H1 expression positively correlated with disease severity of OLP. It is suggested that Th1 dominant inflammatory situation might contribute to the high expression of PD-1 and B7-H1 in OLP. Blockade of PD-1/B7-H1 pathway significantly increased the proliferation, and IFN-γ and IL-2 production of T cells.
  
  
  CONCLUSIONS
  PD-1/B7-H1 pathway may play an important role in negatively modulating T cell-mediated immune response in OLP, and provide the rationale to employ B7-H1 expression on peripheral blood T cells as a marker of severity of OLP and to develop agonists targeting PD-1/B7-H1 pathway as a promising immunotherapeutic strategy for OLP.
authors.affiliation: The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST), School & Hospital of Stomatology, Wuhan University, Wuhan, People's Republic of China. gordonzhou@tom.com
authors.forename: Gang
authors.initials: G
authors.lastname: Zhou
authors.forename: Jing
authors.initials: J
authors.lastname: Zhang
authors.forename: Xiang-wei
authors.initials: XW
authors.lastname: Ren
authors.forename: Jing-yu
authors.initials: JY
authors.lastname: Hu
authors.forename: Ge-fei
authors.initials: GF
authors.lastname: Du
authors.forename: Xue-yi
authors.initials: XY
authors.lastname: Xu
mesh_terms: D000328:Adult; D000368:Aged; D060890:B7-H1 Antigen / Q000097:blood*; D015415:Biomarkers; D049109:Cell Proliferation; D005260:Female; D006801:Humans; D007249:Inflammation / Q000276:immunology; D007371:Interferon-gamma / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D007376:Interleukin-2 / Q000097:blood; D015847:Interleukin-4 / Q000097:blood; D017676:Lichen Planus, Oral / Q000276:immunology* / Q000378:metabolism; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D061026:Programmed Cell Death 1 Receptor / Q000097:blood / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D015854:Up-Regulation; D055815:Young Adult
chemical_list: D060890:B7-H1 Antigen; D015415:Biomarkers; D007376:Interleukin-2; C105992:PDCD1 protein, human; D061026:Programmed Cell Death 1 Receptor; D016753:Interleukin-10; D015847:Interleukin-4; D007371:Interferon-gamma