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首页> 外文期刊>Cytokine >Lymphotoxin alpha stimulates proliferation and pro-inflammatory cytokine secretion of rheumatoid arthritis synovial fibroblasts.
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Lymphotoxin alpha stimulates proliferation and pro-inflammatory cytokine secretion of rheumatoid arthritis synovial fibroblasts.

机译：淋巴毒素α刺激类风湿关节炎滑膜成纤维细胞的增殖和促炎性细胞因子分泌。

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OBJECTIVE: TNFalpha plays a crucial role in rheumatoid arthritis (RA) by stimulating fibroblast-like synoviocytes (FLS). Lymphotoxin alpha (LTalpha) is a pro-inflammatory cytokine with significant homology to TNFalpha. We compared the effects of both cytokines on cultured RA FLS. METHODS: Receptor expression on RA FLS was analyzed by FACS. Cells were stimulated with LTalpha or TNFalpha and proliferation was measured by [3H]thymidine incorporation and secretion of inflammatory cytokines and metalloproteinase 3 by ELISA. Activation of MAP kinases and Akt was analyzed by Western blotting. Nuclear translocation of NFkappaB was visualized by immunofluorescence. RESULTS: 60-80% and 30-50% of the RA FLS tested expressed TNF receptors I and II, respectively, and 70-75% expressed HVEM. LTalpha induced RA FLS proliferation at the same level of TNFalpha, which was blocked by etanercept. Both LTalpha and TNFalpha induced activation of MAP kinases ERK1/2 and p38 as well as Akt. 95-98% of FLS showed nuclear translocation of NFkappaB after stimulation with either cytokines. LTalpha and TNFalpha were potent to induce secretion of IL-6, IL-8 and metalloproteinase 3 in FLS. CONCLUSION: LTalpha is as effective as TNFalpha in stimulating RA FLS. Blocking both cytokines might allow a better control of inflammation and synovial proliferation in RA.
机译：目的：TNFα通过刺激成纤维样滑膜细胞（FLS）在类风湿性关节炎（RA）中起关键作用。淋巴毒素α（LTalpha）是一种促炎细胞因子，与TNFalpha具有显着同源性。我们比较了两种细胞因子对培养的RA FLS的影响。方法：应用流式细胞仪分析RA FLS的受体表达。用LTalpha或TNFalpha刺激细胞，并通过[3H]胸苷掺入和ELISA法测定炎症细胞因子和金属蛋白酶3的分泌来测定增殖。通过蛋白质印迹分析MAP激酶和Akt的活化。通过免疫荧光观察NFkappaB的核易位。结果：60-80％和30-50％的RA FLS分别表达TNF受体I和II，70-75％表达HVEM。 LTalpha以相同水平的TNFalpha诱导RA FLS增殖，这被etanercept阻断。 LTalpha和TNFalpha均可诱导MAP激酶ERK1 / 2和p38以及Akt活化。 95-98％的FLS在任一细胞因子刺激后均显示NFkappaB的核易位。 LTalpha和TNFalpha可以有效诱导FLS中IL-6，IL-8和金属蛋白酶3的分泌。结论：LTalpha在刺激RA FLS方面与TNFalpha一样有效。阻断两种细胞因子可能会更好地控制RA中的炎症和滑膜增生。

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