Further, it is well established that IL-10 is a principal anti-inflammatory mediator for many auto-inflammatory diseases including IBD and multiple sclerosis and the animal model experimental autoimmune encephalomyelitis (MS/EAE).29 It has also been shown that naive IL-10−/− mice have a higher number of T cells with autoreactive T cell receptors (TCR) in their lymphoid organs.30 Therefore, we hypothesized that C. jejuni-induced autoimmune response in vivo is mediated by IL-4 and Siglec-1 axes, and these responses are amplified in the absence of IL-10. The gene discussed is IL10; the disease is experimental autoimmune encephalomyelitis.