摘要
Abstract
Objective To analyze the effects of PKCδ and MALT1 on Th 17 cell level,inflammatory factor level and mRNA expression level in peripheral blood mononuclear cells for HIV-TB co-infection patients.Methods From June 2021 to August 2022,4 patients with HIV-TB co-infection were collected from the First People's Hospital of Kashgar.Peripheral blood mononuclear cells(PBMC)were isolated and cultured and divided into blank control group and B106 group[PKCδ inhibitor(B106)treated cells],MI-2 group[MALT1 inhibitor(MI-2)treated cells],B106+MI-2 group[PKCδ inhibitor(B106)and MALT1 inhibitor(MI-2)treated cells]three experimental groups.The level of Th17 cells was detected by flow cytometry.ELISA was used to detect the levels of IL-6,IL-17,IL-23,IFN-γ,TNF-α,IL-10 and IL-22,and qPCR was used to detect the mRNA expression levels of MALT1,Iκbα,P65,IL-17 and IL-23.The effect of PKCδ and MALT1 on cellular immune response in HIV-TB co-infected patients was explored,and its mechanism was preliminarily analyzed.Results The number of Th 17 cells in the three experimental groups was higher than that in the control group,and the difference was statistically significant(P＜0.05).The concentrations of IL-6,IL-17,IL-23,IFN-γ,TNF-α,IL-10 and IL-22 in the three experimental groups were lower than those in the control group,and the differences were statistically significant(P＜0.05),but there was no significant difference among the three experimental groups(P＞0.05).The mRNA expression levels of IL-17 and IL-23 in the three experimental groups were lower than those in the control group,and the differences were statistically significant(P＜0.05).The expression of MALT1 and P65 in the B106 group was lower than that in the control group,and the expression of Iκbα was higher than that in the control group,the differences were statistically significant(P＜0.05).The expression of Iκbα in the MI-2 group was higher than that in the control group,and the expression of P65 was lower than that in the control group,the differences were statistically significant(P＜0.05).There was no significant difference between the B106+MI-2 group and the other two experimental groups(P＞0.05).Conclusion Inhibition of PKCδ or MALT1 can antagonize the decrease of Th17 cells in HIV-TB co-infected patients,inhibit the inflammatory response of HIV-TB,inhibit the SYK/PKCδ/CARMA1-Bcl10-MALT1(CBM)complex pathway,and antagonize the inflammatory response of HIV-TB by inhibiting the NF-κB inflammatory pathway.关键词
艾滋病/结核病/艾滋病与结核病双重感染/蛋白激酶Cδ/黏膜相关淋巴组织淋巴瘤异位基因1Key words
Acquired immune deficiency syndrome/Tuberculosis/HIV-TB co-infection/Protein kinase Cδ/Mucosa-associated lymphoid tissue lymphoma translocation gene 1分类
基础医学
