Skip to main content
ARS Home » Research » Publications at this Location » Publication #166614
Title: IL-4 AND IL-13 MEDIATED HOST PROTECTION AGAINST INTESTINAL NEMATODE PARASITES.

Author
item FINKELMAN, FRED - U CINCINNATI, OHIO
item SHEA-DONOHUE, TEREZ - U MD BALTIMORE MD
item MORRIS, SUZANNE - U CINCINNATI, OHIO
item GILDEA, LUCY - U CINCINNATI, OHIO
item STRAIT, RICHARD - U CINCINNATI, OHIO
item MADDEN, KATHLEEN - USUHS BETHESDA MD
item Urban, Joseph

Submitted to: Immunological Reviews
Publication Type: Review Article
Publication Acceptance Date: 9/15/2004
Publication Date: 10/30/2004
Citation: Finkelman, F., Shea-Donohue, T., Morris, S., Gildea, L., Strait, R., Madden, K., Urban Jr, J.F. 2004. IL-4 and IL-13 mediated host protection against intestinal nematode parasites. Immunological Reviews 201:139-155.

Interpretive Summary:

Technical Abstract: The vertebrate immune system has evolved to defend against a spectrum of infectious pathogens that ranges from sub-microscopic viruses that reside within host cells to worms that can be several meters in length and live in the host's gut, lymphatics, vasculature and subcutaneous tissues. Survival and replication strategies employed by different pathogens include commandeering host mechanisms for producing proteins and polynucleotides (viruses); obtaining nutrients from host cells, secretions and debris (many bacteria, protozoa,and helminths); and eating the host or sharing ingesta from the inside (some intestinal worms). Host responses to these different parasites can result in rapid elimination with little self-damage, elimination with self-damage worse than any damage directly induced by the parasite, benign coexistence, and an absent or ineffectual response that allows the parasite to severely damage or kill the host. To be successful, the host must: 1) recognize the parasite as foreign; 2) activate effector mechanisms that either eliminate the parasite or severely limit the parasite's ability to induce injury; and 3) limit the activation of effector mechanisms that can cause self-damage, particularly effector mechanisms that have little ability to damage or contain the relevant parasite. The overall thesis of this review is that the coupling of optimal host protection with minimal self-injury is mediated by the polarization of cytokine-secreting effector cells into cells that protect against most members of a particular parasite set without adversely affect host integrity.