神经纤毛蛋白-1（NRP-1）在原发免疫性血小板减少症发病机制中的作用

OBJECTIVE: To explore the relationship between the expression of neuropilin-1（NRP-1）on Treg cells and its ligands semaphorins-3A（Sema3A）, transforming growth factor-β(1)（TGF-β(1)）as well as the balance of type 1 helper T cells（Th(1)）and type 2 helper T cells（Th(2)）cells. METHODS: This study enrolled 62 patients with immune thrombocytopenia（ITP; 33 and 29 newly diagnosed and chronic ITP, respectively）from March 2014 to May 2015. Consequently, 30 healthy people in the same period were selected as the normal control group. The expression of NRP-1 in Treg cells was detected via flow cytometry. The Sema3A, TGF-β(1), IFN-γ, and IL-4 levels in plasma were detected by enzyme-linked immunosorbent assay. The real-time polymerase chain reaction technique was used to detect the mRNA expression levels of NRP-1, Sema3A, and TGF-β(1). The one-way analysis of variance and independent sample t-test was used for comparison between three and two groups, respectively. Correlations among the mRNA expression levels of NRP-1, Sema3A, and TGF-β(1) were assessed via Spearman correlation coefficients. RESULTS: Treg cells in the newly diagnosed ITP group significantly increased compared with those in the chronic ITP and normal control groups. The expression of NRP-1 decreased［（0.15 ± 0.03）％,（0.33 ± 0.15）％, and（0.46 ± 0.06）％; P<0.01］, the plasma Sema3A level increased［（8.10 ± 1.32）µg/L,（7.41±1.30）µg/L, and（2.88±0.82）µg/L; P<0.01］, and the plasma TGF-β(1) level decreased［（16.50±3.36）µg/L,（35.17 ± 10.26）µg/L, and（41.00 ± 10.02）µg/L; P<0.01］. Moreover, the level of plasma IFN-γ increased［（17.21+2.80）ng/L,（10.23+1.59）ng/L, and（8.18+3.27）ng/L; P<0.01］, and the ratios of Th(1)/Th(2)（IFN-γ/IL-4）increased（1.29±0.30, 0.72±0.16, and 0.61±0.27; P<0.01）. The mRNA expressions of NRP-1 and Sema3A in the newly diagnosed ITP and chronic ITP groups were lower than that in the normal control group（P<0.01）. Consequently, the NRP-1 mRNA expression was positively correlated with Sema3A and TGF-β(1) mRNA expression in the newly diagnosed ITP group. CONCLUSION: NRP-1 played an essential role in the pathogenesis of ITP.