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Year : 2018  |  Volume : 43  |  Issue : 3  |  Page : 119-124

T helper 1/T helper 2-associated chemokine and chemokine receptor expression in immune thrombocytopenia

1 Department of Clinical and Chemical Pathology, Faculty of Medicine, Cairo University, Cairo, Egypt
2 Department of Pediatrics, Faculty of Medicine, Cairo University, Cairo, Egypt

Correspondence Address:
Nadia I Sewelam
50 Mekias Street, Manial Alrouda, Cairo, 11451
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ejh.ejh_12_18

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Background Immune thrombocytopenia (ITP) is an acquired immune disorder. Chemokines have complicated role in different autoimmune disorders including ITP. C-C motif chemokine ligand 2 (CCL2) chemokine represents a T helper (Th)2 polarizing chemokine, whereas C-X-C motif chemokine receptor 3 (CXCR3) and C-C motif chemokine receptor 2 (CCR2) represent chemokine members with Th1 polarization effect on the immune system. ITP is associated with an imbalance in Th1/Th2 ratio and favors Th1 polarization. This study aimed to explore the role of CCL2 and its receptor CCR2 in addition to CXCR3 receptor gene expression in the pathogenesis and severity of ITP. Participants and methods Expression of CCL2, CCR2, and CXCR3 was assayed using real-time quantitative polymerase chain reaction in peripheral blood mononuclear cells of 21 normal healthy participants and 68 patients with ITP: 24 acute cases, 25 chronic responder cases, and 19 chronic non-responder cases. Results Acute ITP group showed a 1.85 median fold change in CCL2 gene expression from the control group. CCR2 and CXCR3 showed a higher median fold change from the control group in acute ITP (7.36 and 5.42, respectively) and in chronic non-responder patients (3.38 and 4.32, respectively), whereas the chronic responder patients showed the least changes (1.63 and 2.35, respectively). There was no significant difference in chemokine or chemokine receptors gene expression between different ITP groups (P>0.05). Statistically significant positive correlations were detected between CCL2 and CCR2 (r=0.453, P<0.001) and between CXCR3 and CCR2 (r=0.583, P<0.001) among patients with ITP. Conclusion CCR2 and CXCR3 but not CCL2 may have a role in ITP pathogenesis. Further studies investigating the role of the complicated chemokine network may help better understanding of ITP pathogenesis.

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