title: Elevated profiles of Th22 cells and correlations with Th17 cells in patients with immune thrombocytopenia.
abstract: T-helper (Th) 22 and Th17 cells are implicated in the pathogenesis of autoimmune diseases. However, the role of Th22 cells in the pathophysiology of immune thrombocytopenia (ITP) remains unclear. Th22, Th17 and Th1 cells in both ITP patients and healthy controls were examined by flow cytometry. Plasma interleukin-22 (IL-22) level was measured by enzyme linked immunosorbent assay (ELISA). Signal transducers and activators of transcription 3 (STAT-3) and transcription factor RAR-related organ receptor C (RORC) messenger RNA (mRNA) expressions were examined by quantitative reverse transcription polymerase chain reaction (RT-PCR). Th22 cells, Th17 cells, Th1 cells and plasma IL-22 were significantly higher in ITP patients than in healthy controls. Moreover, Th22 cells showed a positive correlation with the levels of plasma IL-22 as well as Th17 and Th1 cells in ITP patients. Significant up-regulations of both STAT-3 and RORC transcription factors were also observed. Additionally, the percentage of Th22 cells was higher in autoantibody-negative ITP patients than in autoantibody-positive patients. Our results demonstrate a possible role of Th22 cells in ITP, and thus, the blockade of IL-22 may be a reasonable therapeutic strategy for ITP.
authors.affiliation: Department of Hematology, Qilu Hospital of Shandong University, Jinan 250012, PR China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Hu
authors.forename: Haiyan
authors.initials: H
authors.lastname: Li
authors.forename: Lei
authors.initials: L
authors.lastname: Zhang
authors.forename: Baozhong
authors.initials: B
authors.lastname: Shan
authors.forename: Xingfang
authors.initials: X
authors.lastname: Xu
authors.forename: Hong
authors.initials: H
authors.lastname: Li
authors.forename: Xinguang
authors.initials: X
authors.lastname: Liu
authors.forename: Shuqian
authors.initials: S
authors.lastname: Xu
authors.forename: Shuang
authors.initials: S
authors.lastname: Yu
authors.forename: Daoxin
authors.initials: D
authors.lastname: Ma
authors.forename: Jun
authors.initials: J
authors.lastname: Peng
authors.forename: Ming
authors.initials: M
authors.lastname: Hou
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001323:Autoantibodies / Q000276:immunology; D015551:Autoimmunity; D001792:Blood Platelets / Q000276:immunology* / Q000473:pathology; D016022:Case-Control Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007378:Interleukins / Q000097:blood / Q000276:immunology; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000097:blood / Q000235:genetics / Q000276:immunology; D010976:Platelet Count; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050796:STAT3 Transcription Factor / Q000097:blood / Q000235:genetics / Q000276:immunology; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology / Q000473:pathology*; D058504:Th17 Cells / Q000276:immunology / Q000473:pathology*; D013921:Thrombocytopenia / Q000097:blood / Q000276:immunology / Q000473:pathology*; D015854:Up-Regulation; D000097043:Interleukin-22
chemical_list: D001323:Autoantibodies; D007378:Interleukins; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D050796:STAT3 Transcription Factor; D000097043:Interleukin-22; C539900:RORC protein, human; C494086:STAT3 protein, human