title: Th17 cells facilitate the humoral immune response in patients with acute viral myocarditis.
abstract: BACKGROUND
  Recently, the Th17 cell, a newly determined CD4+Th subset, was reported to participate in the inflammation of myocarditis combined with Th1 cells, and this study aimed to explore whether it was involved in the Th2 cell-mediated humoral immunity in viral myocarditis.
  
  
  METHODS
  A total of 34 patients, including 16 acute viral myocarditis (AVMC) and 18 dilated cardiomyopathy (DCM) having a history of AVMC, were enrolled for this study besides 18 healthy volunteers.
  
  
  RESULTS
  The frequencies of Th17 and Th1 cells, especially Th17 cells in AVMC patients, while those of Th1 and Th2 cells, especially Th2 cells in DCM group, were all increased significantly compared with those in healthy volunteers (P < 0.01), with no changes of Th2 cells in AVMC and Th17 cells in DCM groups. The similar results were also observed in Th cell cytokines (IL-17, INF-gamma, and IL-4) and key transcript factors (RORgammat, T-bet, and GATA-3). Meanwhile, antiheart antibodies (AHA) of IgG type were found in 15 (93.8%) patients with AVMC and ten (55.6%) cases with DCM, accompanied by the higher expression of IL-17R on B cells and the frequencies of B cells than those in healthy controls (P < 0.01 in AVMC and P < 0.05 in DCM, respectively) who had no AHA. Furthermore, both of the B cell activities in AVMC and DCM groups were elevated and positively correlated to serum IL-17 (R = 0.66, P < 0.01) and IL-4 (R = 0.47, P < 0.05) respectively, with no correlation to INF-gamma.
  
  
  CONCLUSIONS
  It was Th17 cells but not Th2 cells that helped the B cells to produce AHA in AVMC and not until at the late phase of viral myocarditis could Th2 cells play the important role in mediating humoral response.
authors.affiliation: Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Huazhong University of Science and Technology, Wuhan, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Yuan
authors.forename: Ai-Lin
authors.initials: AL
authors.lastname: Cao
authors.forename: Miao
authors.initials: M
authors.lastname: Yu
authors.forename: Qiong-Wen
authors.initials: QW
authors.lastname: Lin
authors.forename: Xian
authors.initials: X
authors.lastname: Yu
authors.forename: Jing-Hui
authors.initials: JH
authors.lastname: Zhang
authors.forename: Min
authors.initials: M
authors.lastname: Wang
authors.forename: He-Ping
authors.initials: HP
authors.lastname: Guo
authors.forename: Yu-Hua
authors.initials: YH
authors.lastname: Liao
mesh_terms: D000208:Acute Disease; D000328:Adult; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D015704:CD4 Antigens / Q000096:biosynthesis; D002311:Cardiomyopathy, Dilated; D016207:Cytokines / Q000097:blood; D005260:Female; D006801:Humans; D056724:Immunity, Humoral; D007074:Immunoglobulin G / Q000097:blood*; D008297:Male; D009205:Myocarditis / Q000097:blood / Q000150:complications / Q000276:immunology* / Q000503:physiopathology; D009206:Myocardium / Q000276:immunology; D053722:Receptors, Interleukin-17 / Q000235:genetics / Q000378:metabolism; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D014777:Virus Diseases / Q000097:blood / Q000150:complications / Q000276:immunology* / Q000503:physiopathology
chemical_list: D015704:CD4 Antigens; D016207:Cytokines; D007074:Immunoglobulin G; D053722:Receptors, Interleukin-17