Submitted to: Avian Immunology Group Meeting
Publication Type: Abstract Only
Publication Acceptance Date: August 22, 2008
Publication Date: N/A
In mammals, the IL-17 family of cytokines (IL-17A-F) has a very distinct expression pattern and a different biological function. IL-17 is mainly secreted by activated CD4+ T cells and has been implicated in autoimmune and inflammatory diseases. IL-17 has been shown to exert an important role in host defense mechanisms against viral or bacterial infections. In our previous report, we have demonstrated that a 917-bp cDNA that we identified in our chicken EST library prepared from intestinal intraepithelial lymphocytes (IELs) of Eimeria-infected chickens is the avian homologue of mammalian IL-17A with a molecular mass of 18.9 kDa and 6 cysteine residues conserved with mammalian IL-17. Chicken IL-17A (chIL-17A) shared 37%–46% amino acid sequence identity to the previously described mammalian homologs and chIL-17A induced IL-6 production by chicken embryonic fibroblasts, suggesting a functional role for the cytokine in avian immunity. Recently, we have identified IL-17D cDNA from a chicken testis cDNA library which consisted of a 348 nucleotide sequence encoding an open reading frame of 116 amino acids with a predicted molecular mass of 13.4 kDa. Comparison of the deduced amino acid sequence of chIL-17D with homologous proteins from human, mouse and opossum revealed 64%, 53% and 76% identity respectively, including six conserved cysteine residues present in the mammalian polypeptides. Endogenous chIL-17D mRNA was present in all organs examined with highest levels in pancreas, thymus and lung. Following E. maxima infection, chIL-17D transcript levels were increased in intestinal IELs, bursa, lung, and spleen but decreased in the thymus. Among IEL subpopulations, infected chickens expressed greater levels of the chIL-17D mRNA in CD4+, CD8+ and TCR1+ cells but decreased expression in TCR2+ cells. Collectively, these results suggest that chL-17D plays an important role in local gut innate immune responses.