BACKGROUND:Triggering receptor expressed on myeloid cel s 2 (TREM-2) is highly expressed throughout the synovial tissue in active rheumatoid arthritis patients, but the role of TREM-2 in the pathogenesis of rheumatoid arthritis stil remains unclear.
OBJECTIVE:To explore the TREM-2 expression in the synovial tissue of col agen type II-induced arthritis rats.
METHODS:The col agen-induced arthritis models were established in rats. The activity indicators and pathological changes of arthritis synovial were dynamical y observed. The mRNA levels of TREM-2, tumor necrosis factor-α, interleukin-1β, and interleukin-10 were detected in synovial tissue of rats by RT-PCR. The protein expression and location of TREM-2 were measured with western blot assay and immunohistochemistry, respectively.
RESULTS AND CONCLUSION:At day 13 after immunization, the paws of model rats appeared red and swel ing, the arthritis index scores were increased (P<0.01). At day 19-25 after immunization, the inflammation reached the peak. Hematoxylin-eosin staining showed that, the synovium of col agen-induced arthritis rats were proliferated and were infiltrated by inflammatory cel s, cartilage was destroyed. Compared with the control group, the expression of TREM-2 mRNA and protein, the mRNA levels of tumor necrosis factor-αand interleukin-1βin synovial tissue of the model rats were significantly increased (P<0.05 or P<0.01), while interleukin-10 mRNA expression was significantly decreased (P<0.05). Experimental findings indicate that, TREM-2 is a crucial inflammatory regulator and the increasing expression of TREM-2 plays an important role in the pathogenesis of col agen-induced arthritis.

Objective:To investigate the combining therapy which not only have cured effect but also can uphold and improve the NPC patient′s immunity function after radiotherrapy and chemotherapy.Method:90 cases randomly divided into 3 groups ①Local group (local injected with IL-2 +radiotherapy+chemotherapy);②General group(ivdrip with IL-2+radiotherapy+chemotherapy);③convention group(radiotherapy+chemotherapy).Checked and observed the immunity function around the immunotherapy and after the radiotherapy and chemotherapy.Result:Cellular immunity of 3 groups are lower and humoral immunity are hypetuntion than normal person.After treated with IL-2 the cellular immunity improves but there′s no great change of the humoral immunity. The immune status of the immune groups have not obvious change than before radiotherapy,at the same time,the cellular immunity of the convention group cut down and the humoral immunity doesn′t change obviously.Conclusion:①It has some effect to uphold and improve the NPC patient′s immunity function to treat with small dosage of IL-2 before radiotherapy and chemotherapy,general treatment is better than local injection;②The three therapies have not great influence on the patient′s humoral immunity.

AIM: To investigate the effects of transient receptor potential channel 6 (TRPC6) on the proliferation of rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS) induced by IL-1β.METHODS: The mRNA expression of TRPC6 in synovial tissues from RA or OA patients was studied by RT-qPCR.RA-FLS were cultured by enzyme digestion and tissue adhesion methods.The method of flow cytometry was applied to identify the RA-FLS.RA-FLS were treated with different concentrations (0, 0.25, 0.5, 1, 2, 4, 8 and 16 μg/L) of IL-1β for 36 h.The cell viability was examined by CCK-8 assay.RA-FLS were incubated with IL-1β (16 μg/L) for different time (12, 24, 36, 48, 60 and 72 h), and the cell viability was measured by CCK-8 assay.The interference efficiency of TRPC6-siRNA was determined by RT-qPCR and Western blotting.After incubation in the presence or absence of IL-1β medium, the cell viability, the percentage of EdU-positive cells and the percentage of (G2/M+S) phase were measured by CCK-8 assay, EdU labeling assay and flow cytometry, respectively.RESULTS: The mRNA expression of TRPC6 was found in synovial tissue with higher levels in RA patients than that in OA patients.TRPC6-siRNA significantly decreased the mRNA and protein expression of TRPC6 (P<0.05).When RA-FLS were treated with IL-1β, the proliferation of RA-FLS was increased (P<0.05).The differences of the cell viability, the percentage of EdU-positive cells and the (G2/M+S) phase percentage between TRPC6-siRNA group and blank control group or NC-siRNA group were significant, in the presence of IL-1β (P<0.05).However, they were not significant in the absence of IL-1β.CONCLUSION: TRPC6 is involved in the proliferation of RA-FLS induced by IL-1β.Silencing of TRPC6 gene inhibits the growth of RA-FLS induced by IL-1β.