title: Elevated interleukin-21 correlated to Th17 and Th1 cells in patients with immune thrombocytopenia.
abstract: BACKGROUND
  Interleukin-21 (IL-21) is critical in the development of autoimmune diseases. The role of IL-21 in the pathogenesis of immune thrombocytopenia (ITP) remains unknown.
  
  
  METHODS
  We examined the expression of IL-21, IL-17, and interferon (IFN)-gamma in ITP patients and controls by enzyme-linked immunosorbent assay and flow cytometry. Detection of specific anti-platelet GPIIb/IIIa and/or GPIb/IX autoantibodies was measured by modified monoclonal antibody specific immobilization of platelet antigens.
  
  
  RESULTS
  IL-21 was expressed on both CD3(+)CD8(-) T cells and CD3(+)CD8(+) T cells by flow cytometry. Plasma IL-21 level and the percentage of CD3(+)CD8(-)IL-21(+) T cells and CD3(+)CD8(+)IL-21(+) T cells were significantly elevated in ITP patients compared to controls. The percentage of CD3(+)CD8(-)IL-17(+) T (Th17), CD3(+)CD8(-)IFN-gamma(+) T (Th1), and CD3(+)CD8(+)IFN-gamma(+) T (Tc1) cells also significantly increased in ITP patients. Moreover, we found a significant positive correlation between CD3(+)CD8(-)IL-21(+) T cells and Th17 cells. In addition, a positive correlation between CD3(+)CD8(-)IL-21(+) T cells and Th1 cells was also found.
  
  
  CONCLUSIONS
  Together, our results indicated a possible role of IL-21 in ITP patients correlated to Th17 and Th1 cells, and blockade of IL-21 may be a reasonable therapeutic strategy for ITP especially those with active disease.
authors.affiliation: Haematology Oncology Centre, Qilu Hospital, Shandong University, Jinan, Shandong, People's Republic of China.
authors.forename: Xiaojuan
authors.initials: X
authors.lastname: Zhu
authors.forename: Daoxin
authors.initials: D
authors.lastname: Ma
authors.forename: Jingbo
authors.initials: J
authors.lastname: Zhang
authors.forename: Jun
authors.initials: J
authors.lastname: Peng
authors.forename: Xun
authors.initials: X
authors.lastname: Qu
authors.forename: Chunyan
authors.initials: C
authors.lastname: Ji
authors.forename: Ming
authors.initials: M
authors.lastname: Hou
mesh_terms: D000293:Adolescent; D000328:Adult; D015703:Antigens, CD / Q000096:biosynthesis; D001323:Autoantibodies / Q000097:blood; D002469:Cell Separation; D002478:Cells, Cultured; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis* / Q000235:genetics; D020381:Interleukin-17 / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D007378:Interleukins / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D008297:Male; D008875:Middle Aged; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000276:immunology / Q000378:metabolism; D019038:Platelet Glycoprotein GPIb-IX Complex / Q000276:immunology / Q000378:metabolism; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000097:blood / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D000098546:Interleukin-21
chemical_list: D015703:Antigens, CD; D001323:Autoantibodies; D020381:Interleukin-17; D007378:Interleukins; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D019038:Platelet Glycoprotein GPIb-IX Complex; C032193:glycoprotein receptor GPIb-IX; D007371:Interferon-gamma; D000098546:Interleukin-21