The severity of experimental arthritis is independent of IL-36 receptor signaling.
The severity of experimental arthritis is independent of IL-36 receptor signaling.
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DOI：
10.1186/ar4192
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发表时间：
2013-03-01
影响因子：
4.9
通讯作者：
Gabay C
中科院分区：
文献类型：
--
作者：
Lamacchia C;Palmer G;Rodriguez E;Martin P;Vigne S;Seemayer CA;Talabot-Ayer D;Towne JE;Gabay C
白细胞介素（IL）-36是指与IL-36受体（IL-36 R）结合的三种相关IL-1家族细胞因子IL-36α、IL-36β和IL-36γ。IL-36在皮肤和肺中发挥促炎作用并刺激T细胞应答。在本研究中，我们研究了IL-36 R及其配体在实验性关节炎中的表达和功能。根据标准方案诱导胶原诱导的关节炎（CIA）、抗原诱导的关节炎（AIA）和K/BxN血清转移诱导的关节炎。通过RT-qPCR测定CIA小鼠关节中IL-36 R及其配体的信使RNA水平。在关节炎发作时，向患有CIA的小鼠注射阻断性单克隆抗IL-36 R、阻断性抗IL-1 RI或其同种型匹配的对照抗体。在AIA诱导时还注射抗IL-36 R或对照抗体。最后，在AIA和血清转移诱导的关节炎中检查IL-36 R缺陷型小鼠。通过临床和组织学评分评估关节炎的发展和严重程度。CIA小鼠关节组织中检测到IL-36 R、IL-36 Ra和IL-36γ mRNA，但其水平与关节炎严重程度无关。与抗IL-1 RI抗体治疗相反，注射抗IL-36 R抗体对CIA的发展和严重程度没有影响。抗IL-36 R抗体治疗也未改变AIA中关节炎症和结构损伤的严重程度。最后，AIA和K/BxN血清转移诱导的关节炎的严重程度在IL-36 R缺陷型和野生型小鼠中相似。实验性关节炎的发展和严重程度与IL-36 R信号转导无关。
Interleukin (IL)-36 refers to three related IL-1 family cytokines, IL-36α, IL-36β, and IL-36γ, that bind to the IL-36 receptor (IL-36R). IL-36 exerts proinflammatory effects in skin and lung and stimulates T cell responses. In the present study, we examined the expression and function of IL-36R and its ligands in experimental arthritis. Collagen-induced arthritis (CIA), antigen-induced arthritis (AIA), and K/BxN serum transfer-induced arthritis were induced according to standard protocols. Messenger RNA levels for IL-36R and its ligands in the joints of mice with CIA were determined by RT-qPCR. Mice with CIA were injected with a blocking monoclonal anti-IL-36R, a blocking anti-IL-1RI, or their isotype-matched control antibodies at the time of arthritis onset. Anti-IL-36R or control antibodies were also injected at the time of AIA induction. Finally, IL-36R-deficient mice were examined in AIA and serum transfer-induced arthritis. The development and severity of arthritis were assessed by clinical and histological scoring. IL-36R, IL-36Ra and IL-36γ mRNA were detected in the joints of mice with CIA, but their levels did not correlate with arthritis severity. As opposed to anti-IL-1RI antibody treatment, the injection of an anti-IL-36R antibody was devoid of effect on the development and severity of CIA. The severity of joint inflammation and structural damage in AIA was also unaltered by anti-IL-36R antibody treatment. Finally, the severity of AIA and K/BxN serum transfer-induced arthritis was similar in IL-36R-deficient and wild-type mice. The development and severity of experimental arthritis are independent of IL-36R signaling.
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DOI：
10.1165/rcmb.2009-0315oc
发表时间：
2011-02-01
影响因子：
6.4
作者：
Ramadas, Ravisankar A.;Ewart, Susan L.;LeVine, Ann Marie
通讯作者：
LeVine, Ann Marie
影响因子：
4.8
作者：
Kumar, S;McDonnell, PC;Young, PR
通讯作者：
Young, PR
影响因子：
4.4
作者：
Busfield, SJ;Comrack, CA;Pan, Y
通讯作者：
Pan, Y
影响因子：
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作者：
Chu, Cong-Qiu;Swart, David;Elkon, Keith B.
通讯作者：
Elkon, Keith B.
影响因子：
158.5
作者：
Marrakchi, Slaheddine;Guigue, Philippe;Smahi, Asma
通讯作者：
Smahi, Asma