Th1 (CXCL10) and Th2 (CCL2) chemokine expression in patients with immune thrombocytopenia.

Abstract:

:Immune thrombocytopenia (ITP) is an acquired organ-specific autoimmune disease with a polarization of T(h)1. Both the T(h)1 chemokine CXCL10 and T(h)2 chemokine CCL2 have been studied in several autoimmune diseases, but the status of these chemokines in ITP is still unknown. The aims of this study were to determine the expression of CXCL10 and CCL2 and their receptors, CXCR3 and CCR2, in ITP patients, and to conduct a preliminary study of the pathogenic roles of these factors in ITP. Plasma samples from 49 patients with ITP and 24 normal healthy subjects were assayed for CXCL10 and CCL2 plasma concentration by enzyme-linked immunosorbent assay. Real-time quantitative polymerase chain reaction was performed to determine the mRNA expression of these chemokines and their receptors in the PBMNC of 24 normal controls and 28 active ITP patients as well as splenocytes of nine ITP patients. The CXCL10 levels in the plasma samples from patients with active ITP were significantly higher than those from healthy controls (p = 0.007) and decreased to normal levels in patients with remission ITP. In contrast, CCL2 levels were similar in patients with active disease, patients in remission, and control subjects. PBMNC of patients with active disease expressed more CXCL10 mRNA (p = 0.031) but less CCR2 mRNA (p = 0.005). Lower peripheral platelet count correlated with higher CXCL10 levels and CXCL10/CCL2 ratios. Our study demonstrated that plasma levels of CXCL10 and CXC10/CCL2 ratio were higher in patients with active ITP than in healthy donors, and had an association with platelet counts of the patients. CXCL10 might be a pathogenic factor of this disorder.

journal_name

Hum Immunol

journal_title

Human immunology

authors

Gu D,Chen Z,Zhao H,Du W,Xue F,Ge J,Sui T,Wu H,Liu B,Lu S,Zhang L,Yang R

doi

10.1016/j.humimm.2010.02.010

subject

Has Abstract

pub_date

2010-06-01 00:00:00

pages

586-91

issue

6

eissn

0198-8859

issn

1879-1166

pii

S0198-8859(10)00046-7

journal_volume

71

pub_type

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