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.

Upregulation of CD72 expression on CD19+CD27+ memory B cells by CD40L in primary immune thrombocytopenia

“…CD27 − B cells showed normal or slightly increased expression of CD72. Despite the fact that CD100 expression was reported not to be increased in ITP patients (Zhou et al , ), CD72 dysregulation on CD27 + memory cells was strongly correlated with anti‐platelet antibodies and platelet count. These observations suggested that the increased expression of CD72 on the CD27 + memory B subset is associated with ITP disease activity and autoantibody production.…”

“…Membrane molecules, such as CD22, CD72, the Fcc receptor (FcyR)IIb and PD-1 (also termed PDCD1) negatively regulate B cell receptor (BCR) signalling and prevent overstimulation of the B cells, whereas BCR signalling is up-regulated by membrane molecules such as CD19 (Dal Porto et al, 2004;Tsubata, 2012). Recent studies demonstrated that several of these coreceptors, including CD72, FccRIIb and CD5 have been directly linked to ITP (Iyori et al, 1995;Xu et al, 2008Xu et al, , 2010Liu et al, 2011;Zhou et al, 2012).…”

“…The CD72 mean fluorescence intensity (MFI) was impressively higher on CD5 + than CD5 − B cells in peripheral blood and synovial fluid of rheumatoid arthritis (RA) patients (Jamin et al , ). Our group observed aberrant levels of CD72 mRNA in ITP patients, indicating that CD72 might be involved in the pathogenesis of ITP (Zhou et al , ).…”

Elucidation of the Mechanisms and Molecular Targets of Yiqi Shexue Formula for Treatment of Primary Immune Thrombocytopenia Based on Network Pharmacology

“…It has been shown that allogenic T cell responses could be inhibited through the production of immunoregulatory dendritic cells resulted by silencing RelB (Zhang et al, 2010). The expression of CD72 and IL-2 was decreased whilst the IFN-γ/IL-4 expression was increased in ITP patients (Zhou et al, 2012). Apoptotic process plays an important role in maintenance of normal immune system development, and a failure of apoptotic function has been shown to be associated with the pathogenesis of ITP (Qian et al, 2018).…”

Cellular immune dysfunction in immune thrombocytopenia (ITP)

“…Despite extensive research in recent years attempting to explicate the underlying genetic components associated with ITP, there remains much to be understood. The literature suggests a propensity towards genes associated with the activation of T cells (Anis et al , ; Chen et al , ; Li et al , ,b; Ma et al , ,b, ; Pehlivan et al , ; Rossi et al , ; Saitoh et al , ; Sarpatwari et al , ; Zhou et al , ). The observed polymorphisms included cytokines associated with the activation and survival of CD4 + T cells (Li et al , ,b; Saitoh et al , ; Sarpatwari et al , ), hypomethylation of genes associated with the proinflammatory response (Chen et al , ), CD72 gene polymorphisms and others (Anis et al , ; Pehlivan et al , ; Rossi et al , ; Zhou et al , ), all of which have been suggested to contribute to the pathophysiology of ITP.…”