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- W1758425052 endingPage "96" @default.
- W1758425052 startingPage "83" @default.
- W1758425052 abstract "Exposure to commensal and pathogenic organisms strongly influences our immune system. Exposure to helminths was frequent before humans constructed their current highly hygienic environment. Today, in highly industrialized countries, contact between humans and helminths is rare. Congruent with the decline in helminth infections is an increase in the prevalence of autoimmune and inflammatory disease. It is possible that exclusion of helminths from the environment has permitted the emergence of immune-mediated disease. We review the protective effects of helminths on expression of inflammatory bowel disease, multiple sclerosis, and animal models of these and other inflammatory diseases. We also review the immune pathways altered by helminths that may afford protection from these illnesses. Helminth exposure tends to inhibit IFN-γ and IL-17 production, promote IL-4, IL-10, and TGF-β release, induce CD4(+) T cell Foxp3 expression, and generate regulatory macrophages, dendritic cells, and B cells. Helminths enable protective pathways that may vary by specific species and disease model. Helminths or their products likely have therapeutic potential to control or prevent immune-mediated illness." @default.
- W1758425052 created "2016-06-24" @default.
- W1758425052 creator A5060649766 @default.
- W1758425052 creator A5075038210 @default.
- W1758425052 date "2012-01-01" @default.
- W1758425052 modified "2023-10-13" @default.
- W1758425052 title "Helminth-host immunological interactions: prevention and control of immune-mediated diseases" @default.
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- W1758425052 doi "https://doi.org/10.1111/j.1749-6632.2011.06292.x" @default.
- W1758425052 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3744090" @default.
- W1758425052 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22239614" @default.
- W1758425052 hasPublicationYear "2012" @default.