| First Author | Elliott DE | Year | 2008 |
| Journal | J Immunol | Volume | 181 |
| Issue | 4 | Pages | 2414-9 |
| PubMed ID | 18684931 | Mgi Jnum | J:140190 |
| Mgi Id | MGI:3812256 | Doi | 10.4049/jimmunol.181.4.2414 |
| Citation | Elliott DE, et al. (2008) Colonization with Heligmosomoides polygyrus suppresses mucosal IL-17 production. J Immunol 181(4):2414-9 |
| abstractText | Helminth exposure appears to protect hosts from inappropriate inflammatory responses, such as those causing inflammatory bowel disease. A recently identified, strongly proinflammatory limb of the immune response is characterized by T cell IL-17 production. Many autoimmune type inflammatory diseases are associated with IL-17 release. Because helminths protect from these diseases, we examined IL-17 production in helminth-colonized mice. We colonized mice with Heligmosomoides polygyrus, an intestinal helminth, and analyzed IL-17 production by lamina propria mononuclear cells (LPMC) and mesenteric lymph node (MLN) cells. Colonization with H. polygyrus reduces IL-17A mRNA by MLN cells and inhibits IL-17 production by cultured LPMC and MLN cells. Helminth exposure augments IL-4 and IL-10 production. Blocking both IL-4 and IL-10, but not IL-10 alone, restores IL-17 production in vitro. Colonization of colitic IL-10-deficient mice with H. polygyrus suppresses LPMC IL-17 production and improves colitis. Ab-mediated blockade of IL-17 improves colitis in IL-10-deficient mice. Thus, helminth-associated inhibition of IL-17 production is most likely an important mechanism mediating protection from inappropriate intestinal inflammation. |
