title: CD72 gene expression in immune thrombocytopenia.
abstract: To explore the role of CD72 in the pathogenesis of immune thrombocytopenia (ITP), we detected CD72, Sema4D, IL-2, IL-4, and IFN-γ mRNA expressions and the levels of plasma Sema4D, IL-2, IL-4, IL-6, and IFN-γ in ITP patients (n = 39) and controls (n = 23). The levels of plasma IL-2, IL-4, and IL-6 were assayed by radioimmunoassay, and the levels of plasma IFN-γ and Sema4D were analyzed by enzyme-linked immunosorbent assay. Sema4D, CD72, IL-2, IFN-γ, and IL-4mRNA expressions were analyzed by real-time quantitative reverse-transcription polymerase chain reaction. The expression of CD72 mRNA in ITP patients (n = 23) with active disease was significantly lower than that in patients in remission (p = 0.029) (n = 16) and controls (p = 0.0296) (n = 23). The IFN-γ/IL-4 mRNA (Th1/Th2) expression in ITP patients with active disease and in remission was significantly higher than that in controls (p = 0.0023, p = 0.0125, respectively). The expression of IL-2 mRNA in ITP patients with active disease was significantly lower than that in patients in remission (p = 0.0418) and controls (p = 0.004). The level of plasma IL-2 in ITP patients with active disease was significantly lower than that in patients in remission (p = 0.0029) and controls (p = 0.0101). The levels of plasma IL-4 in ITP patients with active disease and in remission were significantly higher than that of controls (p = 0.0093, p = 0.0053, respectively). CD72 mRNA expression level might correlate with Sema4D mRNA expression in peripheral blood mononuclear cells and level of plasma IL-2 in active ITP patients (p = 0.024 and p = 0.036). Our findings suggest that CD72 might be involved in the pathophysiological process of the ITP disease by increasing B-cell receptor signals.
authors: State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, People's Republic of China.
authors: Hu
authors: H
authors: Zhou
authors: Ai-Ping
authors: AP
authors: Qi
authors: Hui-Yuan
authors: HY
authors: Li
authors: Li
authors: L
authors: Ma
authors: Jian-Hui
authors: JH
authors: Xu
authors: Feng
authors: F
authors: Xue
authors: Shi-Hong
authors: SH
authors: Lu
authors: Qin-Jun
authors: QJ
authors: Zhao
authors: Ze-Ping
authors: ZP
authors: Zhou
authors: Ren-Chi
authors: RC
authors: Yang
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000097:blood / Q000235:genetics*; D000944:Antigens, Differentiation, B-Lymphocyte / Q000097:blood / Q000235:genetics*; D016022:Case-Control Studies; D003289:Convalescence; D005260:Female; D015870:Gene Expression; D006801:Humans; D007371:Interferon-gamma / Q000097:blood / Q000235:genetics; D007376:Interleukin-2 / Q000097:blood / Q000235:genetics*; D015847:Interleukin-4 / Q000097:blood / Q000235:genetics; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics; D008297:Male; D008875:Middle Aged; D011696:Purpura, Thrombocytopenic / Q000097:blood / Q000235:genetics*; D012333:RNA, Messenger / Q000235:genetics*; D039961:Semaphorins / Q000097:blood / Q000235:genetics*
chemical_list: D015703:Antigens, CD; D000944:Antigens, Differentiation, B-Lymphocyte; C093224:CD100 antigen; C064228:CD72 protein, human; C508598:IL4 protein, human; D007376:Interleukin-2; D015850:Interleukin-6; D012333:RNA, Messenger; D039961:Semaphorins; D015847:Interleukin-4; D007371:Interferon-gamma