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ARS Home » Northeast Area » Beltsville, Maryland (BARC) » Beltsville Agricultural Research Center » Animal Biosciences & Biotechnology Laboratory » Research » Publications at this Location » Publication #292442

Title: Recent progress in the understanding of host immunity to avian coccidiosis: IL-17 family cytokines as the sentinels on the intestinal mucosa

Author
item Lillehoj, Hyun

Submitted to: World Veterinary Poultry Association
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/11/2013
Publication Date: 8/19/2013
Citation: Lillehoj, H.S. 2013. Recent progress in the understanding of host immunity to avian coccidiosis: IL-17 family cytokines as the sentinels on the intestinal mucosa. World Veterinary Poultry Association. 41(3):418-428.

Interpretive Summary:

Technical Abstract: The molecular and cellular mechanisms leading to immune protection against Eimeria avian coccidiosis are complex and include multiple aspects of innate and adaptive immunities. Innate immunity is mediated by various subpopulations of immune cells that recognize pathogen associated molecular patterns through their pattern recognition receptors leading to the secretion of soluble factors with diverse functions. Adaptive immunity, which is important in conferring protection against subsequent reinfections, involves subtypes of T and B lymphocytes that mediate antigen-specific immune responses. Recently, global gene expression microarray analysis has been used in an attempt to dissect this complex network of immune cells and molecules during avian coccidiosis. These new studies emphasized the uniqueness of the innate immune response to Eimeria infection, and directly led to the discovery of previously uncharacterized host genes and proteins whose expression levels were modulated following parasite infection. Among these is the IL-17 family of cytokines. This review highlights recent progress in IL-17 research in the context of host immunity to avian coccidiosis. This talk will review recent progress on our understanding of the role of IL-17.