AIMS Many parasitic helminths are known to alter host immune responses and consequently affect the progression of autoimmune and allergic diseases. The parasitic nematode Trichinella sp has been reported to suppress several experimental diseases in rodents, including experimental autoimmune encephalomyelitis, type 1 diabetes, colitis, airway inflammation and autoimmune arthritis. We tried to clarify requirement of Th2 cytokines in the anti-arthritic effects of Trichinella spiralis (Ts) against collagen-induced arthritis (CIA). METHODS AND RESULTS We infected Ts and then induced CIA in STAT6KO DBA/1 mice, comparing the disease progression with that in wild-type (WT) DBA/1 mice, Ts significantly mitigated arthritis in WT mice, in addition to the impairment of anti-type II collagen (IIC) IgG production in a subclass-independent manner. The genetic absence of STAT6 in the mice did not abrogate the anti-arthritic effects of Ts. Alteration of splenic cytokines was not related to the anti-arthritic effects of the parasite. Moreover, lack of IL-10 did not abrogate the anti-arthritic effects of Ts. CONCLUSION Our results suggest that the anti-arthritic effects of Ts do not require host Th2 signals.

中文翻译：

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Th2信号对于旋毛虫在小鼠中的抗关节炎作用不是必需的。

目的已知许多寄生虫蠕虫会改变宿主的免疫反应，从而影响自身免疫和过敏性疾病的进展。据报道，寄生线虫旋毛虫​​可抑制啮齿动物的几种实验疾病，包括实验性自身免疫性脑脊髓炎，1型糖尿病，结肠炎，气道炎症和自身免疫性关节炎。我们试图阐明在旋毛虫（Ts）对胶原诱导的关节炎（CIA）的抗关节炎作用中Th2细胞因子的需求。方法和结果我们在STAT6KO DBA / 1小鼠中感染了Ts，然后诱导了CIA，将其与野生型（WT）DBA / 1小鼠的疾病进展进行了比较，Ts显着减轻了WT小鼠的关节炎，此外还损害了抗II型II型胶原（IIC）IgG的产生具有亚类独立性。小鼠中STAT6的遗传缺失并未消除Ts的抗关节炎作用。脾细胞因子的改变与寄生虫的抗关节炎作用无关。此外，缺乏IL-10并不能消除Ts的抗关节炎作用。结论我们的结果表明Ts的抗关节炎作用不需要宿主Th2信号。