Department of Rheumatology, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia.
Department of Rheumatology, Westmead Hospital, Sydney, 2145, Australia.
Antiinflamm Antiallergy Agents Med Chem. 2023;21(3):188-193. doi: 10.2174/1871523022666230201144553.
The in vitro effects of commonly used first-line anti-arthritic drugs on early stages of T-cell activation were examined.
The 2B4.11 murine T cell hybridoma cell line recognizing pigeon cytochrome c (PCC) as the antigen was co-cultured with the histocompatible antigen presenting B cell hybridoma line LK35.2, PCC, and anti-arthritic drugs, including methotrexate, hydroxychloroquine, salazopyrine, cyclosporin, and leflunomide. After 16 hours of incubation, the supernatant was removed, and cytokines were assayed.
Anti-arthritic drugs inhibited the production of pro-inflammatory cytokines IL-2, IL-6, IFN-γ, GM-CSF, and TNF-α (Th1 cytokines) to a varying extent. Surprisingly, leflunomide, salazopyrine, prednisone and indomethacin as well as blocking Th1 cytokines, stimulated the production of the anti-inflammatory cytokine IL-10, a Th2 cytokine.
Anti-arthritic medications can inhibit the production of pro-inflammatory cytokines and in some cases, incite a Th2 response that could potentially inhibit the progression of the immune response.
研究常用一线抗风湿药物对 T 细胞活化早期阶段的体外影响。
用识别 pigeon cytochrome c(PCC)作为抗原的 2B4.11 鼠 T 细胞杂交瘤细胞系与同种相容的抗原呈递 B 细胞杂交瘤系 LK35.2、PCC 和抗风湿药物(包括甲氨蝶呤、羟氯喹、柳氮磺胺吡啶、环孢素和来氟米特)共同培养。孵育 16 小时后,去除上清液并检测细胞因子。
抗风湿药物不同程度地抑制了促炎细胞因子 IL-2、IL-6、IFN-γ、GM-CSF 和 TNF-α(Th1 细胞因子)的产生。令人惊讶的是,来氟米特、柳氮磺胺吡啶、泼尼松和吲哚美辛以及阻断 Th1 细胞因子的药物,刺激了抗炎细胞因子 IL-10(Th2 细胞因子)的产生。
抗风湿药物可以抑制促炎细胞因子的产生,在某些情况下,还会引发 Th2 反应,从而可能抑制免疫反应的进展。