Helminths, as complex pathogens, possess a large number of different epitopes, some of which may be similar to the epitopes of the host. Besides being the cause for the activation of self-reactive immune cells, molecular mimicry may also be the cause for the expansion of regulatory T cells, crucial for the host tolerance of self-antigens. Amelioration of experimental autoimmune encephalomyelitis (EAE), animal model of multiple sclerosis (MS), caused by Trichinella spiralis infection or application of its muscle larvae excretory-secretory products (ES L1), was achieved through activation of Th2 and regulatory responses. The present study aimed to reveal whether the cause of observed immunomodulation could be the existence of shared epitopes between ES L1 antigens and auto-antigens. Serum samples from 92 MS patients were tested in Western blot for the reactivity toward components of ES L1. Immunoglobulins from the sera of MS patients recognized several ES L1 components, but 45, 49 and 58 kDa proteins dominated others by the frequency of interaction. According to the logistic regression analysis, these interactions were statistically significantly associated with MS, regardless of the disease phenotype or severity. Selected molecules might share homology with self-antigens and as such are worthy of further investigation in terms of potential immunomodulatory capacity and involvement in the parasite's provoked amelioration of EAE.
Keywords: Molecular mimicry; Multiple sclerosis; Trichinella spiralis antigens.
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