Th2 signals are not essential for the anti-arthritic effects of Trichinella spiralis in mice.

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.