title: Differentiation and recruitment of IL-22-producing helper T cells stimulated by pleural mesothelial cells in tuberculous pleurisy.
abstract: BACKGROUND
  IL-22-producing helper T cells (Th22 cells) have been reported to be involved in tuberculosis infection. However, differentiation and immune regulation of Th22 cells in tuberculous pleural effusion (TPE) remain unknown.
  
  
  OBJECTIVE
  To elucidate the mechanism by which Th22 cells differentiate and recruit into the pleural space.
  
  
  METHODS
  The distribution and phenotypic features of Th22 cells in both TPE and blood were determined. The impacts of proinflammatory cytokines and antigen presentation by pleural mesothelial cells (PMCs) on Th22-cell differentiation were explored. The chemoattractant activity of chemokines produced by PMCs for Th22 cells was observed.
  
  
  RESULTS
  Th22 cells were significantly higher in TPE than in blood. IL-1β, IL-6, and/or tumor necrosis factor-α promoted Th22-cell differentiation from CD4(+) T cells. It was found that PMCs expressed CCL20, CCL22, and CCL27, and that TPE and PMC supernatants were chemotactic for Th22 cells. This activity was partly blocked by anti-CCL20, anti-CCL22, and anti-CCL27 antibodies. IL-22 and IL-17 significantly improved PMC wound healing. Moreover, PMCs were able to stimulate CD4(+) T-cell proliferation and Th22-cell differentiation by presenting tuberculosis-specific antigen.
  
  
  CONCLUSIONS
  The overrepresentation of Th22 cells in TPE may be due to pleural cytokines and to PMC-produced chemokines. Our data suggest a collaborative loop between PMCs and Th22 cells in TPE. In particular, PMCs were able to function as antigen-presenting cells to stimulate CD4(+) T-cell proliferation and Th22-cell differentiation.
authors.affiliation: Department of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
authors.forename: Zhi-Jian
authors.initials: ZJ
authors.lastname: Ye
authors.forename: Qiong
authors.initials: Q
authors.lastname: Zhou
authors.forename: Ming-Li
authors.initials: ML
authors.lastname: Yuan
authors.forename: Rong-Hui
authors.initials: RH
authors.lastname: Du
authors.forename: Wei-Bing
authors.initials: WB
authors.lastname: Yang
authors.forename: Xian-Zhi
authors.initials: XZ
authors.lastname: Xiong
authors.forename: Bo
authors.initials: B
authors.lastname: Huang
authors.forename: Huan-Zhong
authors.initials: HZ
authors.lastname: Shi
mesh_terms: D000938:Antigen-Presenting Cells / Q000378:metabolism; D002454:Cell Differentiation; D004848:Epithelium / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007111:Immunity, Cellular; D007378:Interleukins / Q000096:biosynthesis*; D008213:Lymphocyte Activation / Q000276:immunology*; D010994:Pleura / Q000276:immunology / Q000473:pathology*; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D014396:Tuberculosis, Pleural / Q000276:immunology* / Q000473:pathology; D000097043:Interleukin-22
chemical_list: D007378:Interleukins; D000097043:Interleukin-22