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  • Title: Intestinal parasitism terminates self tolerance and enhances neonatal induction of autoimmune disease and memory.
    Author: Agersborg SS, Garza KM, Tung KS.
    Journal: Eur J Immunol; 2001 Mar; 31(3):851-9. PubMed ID: 11241290.
    Abstract:
    Genetic and environmental factors both influence autoimmune disease occurrence, but the identity and mechanism of action of environmental factors are poorly understood. Here we show that pinworm-infected neonatal but not adult mice, injected with an ovarian self peptide of the zona pellucida protein 3 (pZP3) in water and without adjuvant, develop Th2 responses and severe eosinophilic autoimmune ovarian disease. A strong Th2 memory response is recalled when, as adults, the mice are challenged with a regimen that elicits a strong Th1 response in naive adults. The strong Th2 autoimmune response included high levels of IL-4 and IL-5 production by pZP3-specific T cells, and an IgG1-biased autoantibody response. The Th2 response ended promptly upon pinworm eradication, and partially resurfaced upon re-infection. We conclude that the rodent pinworm is an environmental agent that modifies the neonatal response to a self peptide, resulting in termination of the tolerance state and induction of a strong Th2-associated autoimmune disease and T cell memory.
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