title: Pleural mesothelial cells promote expansion of IL-17-producing CD8+ T cells in tuberculous pleural effusion.
abstract: IL-17-producing CD8(+) T lymphocytes (Tc17 cells) have recently been detected in many cancers and autoimmune diseases. However, the possible implication of Tc17 cells in tuberculous pleural effusion remains unclarified. In this study, distribution and phenotypic features of Tc17 cells in both tuberculous pleural effusion (TPE) and peripheral blood from patients with tuberculosis were determined. The effects of proinflammatory cytokines and local accessory cells (pleural mesothelial cells) on Tc17 cell expansion were also explored. We found that TPE contained more Tc17 cells than the blood. Compared with IFN-γ-producing CD8(+) T cells, Tc17 cells displayed higher expression of chemokine receptors (CCRs) and lower expression of cytotoxic molecules. In particularly, Tc17 cells in TPE exhibited high expression levels of CCR6, which could migrate in response to CCL20. Furthermore, IL-1β, IL-6, IL-23, or their various combinations could promote Tc17 cell expansion from CD8(+) T cells, whereas the proliferative response of Tc17 cells to above cytokines was lower than that of Th17 cells. Pleural mesothelial cells (PMCs) were able to stimulate Tc17 cell expansion via cell contact in an IL-1β/IL-6/IL-23 independent fashion. Thus this study demonstrates that Tc17 cells marks a subset of non-cytotoxic, CCR6(+) CD8(+) T lymphocytes with low proliferative capacity. The overrepresentation of Tc17 cells in TPE may be due to Tc17 cell expansion stimulated by pleural proinflammatory cytokines and to recruitment of Tc17 cells from peripheral blood. Additionally, PMCs may promote the production of IL-17 by CD8(+) T cells at sites of TPE via cell-cell interactions.
authors.affiliation: Department of Respiratory Diseases, Key Laboratory of Pulmonary Diseases of Health Ministry, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, 430022, China.
authors.forename: X
authors.initials: X
authors.lastname: Li
authors.forename: Q
authors.initials: Q
authors.lastname: Zhou
authors.forename: W B
authors.initials: WB
authors.lastname: Yang
authors.forename: X Z
authors.initials: XZ
authors.lastname: Xiong
authors.forename: R H
authors.initials: RH
authors.lastname: Du
authors.forename: J C
authors.initials: JC
authors.lastname: Zhang
mesh_terms: D000328:Adult; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D002450:Cell Communication; D049109:Cell Proliferation; D002478:Cells, Cultured; D016207:Cytokines / Q000276:immunology; D003602:Cytotoxicity, Immunologic; D004848:Epithelium / Q000276:immunology* / Q000473:pathology; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000276:immunology; D020381:Interleukin-17 / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010994:Pleura / Q000473:pathology; D010996:Pleural Effusion / Q000276:immunology*; D054399:Receptors, CCR6 / Q000378:metabolism; D058504:Th17 Cells / Q000276:immunology*; D014396:Tuberculosis, Pleural / Q000276:immunology*; D055815:Young Adult
chemical_list: C106311:CCR6 protein, human; D016207:Cytokines; D018836:Inflammation Mediators; D020381:Interleukin-17; D054399:Receptors, CCR6