Candida albicans cell-wall fraction exacerbates collagen-induced arthritis in mice
Candida albicans cell-wall fraction exacerbates collagen-induced arthritis in mice
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DOI：
10.1111/j.1365-3083.2005.01575.x
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发表时间：
2005-04-01
影响因子：
3.7
通讯作者：
Ivanovska, N
中科院分区：
文献类型：
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作者：
Yordanov, M;Tchorbanov, A;Ivanovska, N
免疫系统对大多数病原体产生特异性反应，同时对自身抗原产生耐受性。共生微生物可以表达模仿自身表位的分子结构。在急性感染期间，此类病原体可能会激活自身反应性 T 细胞克隆，从而促进自身免疫。在本研究中，将来自白色念珠菌的 P-巯基乙醇细胞壁组分 (MF) 注射到初始 ICR 和 BALB/c 小鼠的爪子以及患有 II 型牛胶原诱导关节炎 (CIA) 的 ICR 小鼠的爪子中。监测炎症的发展6周。 MF 在 ICR 小鼠中引起注射关节的稳定肿胀和组织病理学变化，其中 T 辅助细胞 I 细胞因子占主导地位。在 BALB/c 菌株中，仅在早期观察到肿胀，没有关节病理学的证据。注射 MF 部分会加剧患有 CIA 的 ICR 小鼠的疾病，这与干扰素 γ 和抗牛 II 型胶原 (bCII) 免疫球蛋白 G2a 抗体的升高有关。这些结果表明 MF 级分中的成分与 bCII 特异性细胞发生交叉反应。
The immune system generates a specific response against most pathogens, while developing tolerance to self-antigens. Commensal micro-organisms can express molecular structures that mimic self-epitopes. During acute infection, such pathogen may activate self-reactive T-cell clones promoting autoimmunity. In the present study, a P-mercaptoethanol cell-wall fraction (MF) from Candida albicans was injected into the paw of naive ICR and BALB/c mice and into the paw of ICR mice with bovine collagen type II-induced arthritis (CIA). Development of inflammation was monitored for 6 weeks. MF provoked a stable swelling and histopathologic changes in the injected joint, with a predominance of T-helper I cytokines in ICR mice. In BALB/c strain, a swelling was observed only in the early period, with no evidence of joint pathology. Injection of the MF fraction exacerbated the disease in ICR mice with CIA, and this was associated with the elevation of interferon-gamma and anti-bovine type II collagen (bCII) immunoglobulin G2a antibodies. These results indicate that component(s) in the MF fraction cross-react with bCII-specific cells.