Objective To investigate the cytokine levels and their clinical significance in pa-tients with inflammatory bowel disease(IBD)complicated by active tuberculosis(ATB)following an-ti-tumor necrosis factor-α(TNF-α)therapy.Methods A retrospective study was conducted in 92 patients with IBD complicated by latent tuberculosis infection.The patients were divided into observa-tion group(37 cases)and control group(55 cases)based on whether they developed ATB.Enzyme-linked immunosorbent assay(ELISA)was used to measure serum cytokine levels,including interfer-on-γ(IFN-γ),interleukin-1 receptor antagonist(IL-1Ra),interleukin-2(IL-2),interleukin-4(IL-4),interleukin-10(IL-10)and interleukin-17(IL-17).Spearman correlation analysis was per-formed to evaluate the associations between cytokine levels and the risk of secondary ATB.Multivari-ate Logistic regression analysis was used to identify the influencing factors for development of ATB in IBD patients treated with anti-TNF-α therapy.Receiver operating characteristic(ROC)curves were plotted to evaluate the predictive value of cytokines for the development of ATB.Results The levels of IFN-γ,IL-1Ra,IL-2 and IL-10 in the observation group were significantly higher than those in the control group(P＜0.05).The levels of IL-4 and IL-17 in the observation group were slightly higher than those in the control group,but the differences were not statistically significant(P＞0.05).Positive correlations were observed between the levels of IFN-γ,IL-1Ra,IL-2 and IL-10 and the risk of secondary ATB(r=0.737,0.586,0.660 and 0.619,respectively;P＜0.05).Serum levels of IFN-γ,IL-1Ra,IL-2 and IL-10 were all independent influencing factors for the de-velopment of ATB in IBD patients treated with anti-TNF-α therapy(P＜0.05).ROC curve analysis revealed that the combination of IFN-γ,IL-1Ra and IL-10 had the highest predictive efficacy for the development of ATB in IBD patients treated with anti-TNF-α therapy,with an area under the curve of 0.996.Conclusion The serum levels of IFN-γ,IL-1Ra,IL-2 and IL-10 are significantly ele-vated in IBD patients complicated by ATB following anti-TNF-α therapy.These cytokines are all in-dependent influencing factors for the development of ATB,and the combination of IFN-γ,IL-1Ra and IL-10 demonstrates the highest predictive efficacy.

Objective:To analyze the expression of human leukocyte antigen G (HLA-G) in human T-cell leukemia virus type 1 (HTLV-1)-positive T cells, and to investigate its role in the occurrence and development of HTLV-1 infection.Methods:The expression of HLA-G in HTLV-1-positive T cell lines (MT2 and MT4) was detected by Western blot and real-time PCR. HLA-G gene in MT2 and MT4 cells was knocked down by siRNA, and the effects of HLA-G on the expression of HTLV-1 Tax and P19 at mRNA and protein levels were detected by Western blot and real-time PCR. Moreover, the changes in cytokine expression in MT2 and MT4 cells were monitored at RNA level after HLA-G gene silencing. The proliferation ability of MT2 and MT4 cells was analyzed by CCK8. Signal transducer and activator of transcription 3 (STAT3) pathway-related proteins were detected by Western blot.Results:Compared with HTLV-1-negative T cells (Jurkat and MOLT4), the expression of HLA-G increased significantly in MT2 and MT4 cells. After knocking down the HLA-G gene with siRNA in MT2 and MT4 cells, the expression of HTLV-1 Tax and P19 at mRNA and protein levels was decreased, and the expression of antiviral cytokines IFN-γ and TNF-α was increased. The proliferation of MT2 and MT4 cells and STAT3 phosphorylation in these cells were decreased.Conclusions:HTLV-1 could induce T cells to overexpress the immune tolerance molecule HLA-G. Silencing HLA-G gene in HTLV-1-positive T cells could promote the production of antiviral cytokines and reduce IL-6 expression and STAT3 phosphorylation, thereby effectively inhibiting the replication of HTLV-1.

【Objective】 To investigate the effect of HLA-G expressed in platelets on Tax protein of human T cell leukemia type 1 virus (HTLV-1). 【Methods】 Platelets were isolated from anticoagulant whole blood, and HLA-G molecule on platelet membrane was detected by flow cytometry. The content of secretory HLA-G before and after platelet lysis was detected by ELISA, HTLV-1 human lymphoma cells MT2 were cultured with platelet lysate (PL). The effect of HLA-G in platelets on the expression of HTLV-1 protein Tax was evaluated by Western blot (WB). 【Results】 Membrane type mHLA-G was highly expressed on the surface of platelet membrane. The expression of secretory sHLA-G (ng/mL) increased after platelet lysis (15.73±1.01) vs (6.65±0.47), the expression of sHLA-G increased with the increase of platelet concentration in a dose-dependent manner. Compared with fetal bovine serum, PL significantly promoted the high expression of HLA-G protein and HTLV-1 virus tax protein in MT2 cells, and the addition of anti-HLA-G antibody to PL could effectively inhibit the expression of Tax and HLA-G protein. 【Conclusion】 High expression of immune tolerance molecule HLA-G on platelets can induce high expression of HTLV-1 protein Tax in human lymphoma cell MT2, which contributes to viral infection.

Objective:To study the expression of human leukocyte antigen G (HLA-G) during human T lymphocytic leukemia virus type 1 (HTLV-1) infection, and to investigate the function and mechanism of HLA-G in HTLV-1 immune escape.Methods:HeLa and THP-1 cells were infected by MT2, a stable HTLV-1 infected cell line. Expression of HLA-G isomers at mRNA and protein levels was detected by qRT-PCR and Western blot, respectively. Flow cytometry was used to detect the expression of HLA-G1. Moreover, transfection and siRNA gene were respectively used to up-regulate and silence HLA-G expression in HeLa cells to observe the changes in the expression of HTLV-1-featured protein Tax on protein level after HTLV-1 infection.Results:HTLV-1 infection could induce differential expression of HLA-G isomers, mainly HLA-G1 and HLA-G5, in HeLa and THP-1 cells. HLA-G expression at both mRNA and protein levels was significantly up-regulated 24 h after HTLV-1 infection. Moreover, the expression of HTLV-1 protein Tax was significantly enhanced in HTLV-1-infected HeLa cells overexpressing HLA-G. An opposite result was obtained when the HLA-G gene in HeLa cells was silenced by siRNA.Conclusions:The immune-tolerant molecule HLA-G was significantly increased in HTLV-1-infected cells, thereby promoting the expression of HTLV-1 viral protein, which led to persistent viral infection.