IL-17A (D1X7L) Rabbit mAb

The IL-17 family of cytokines consists of IL-17A-F, and their receptors include IL-17RA-RE (1). IL-17 cytokines are produced by a variety of cell types including the Th17 subset of CD4+ T cells, as well as subsets of γδ T cells, NK cells, and NKT cells (2). IL-17A and IL-17F, the most well-studied of the IL-17 cytokines, contribute to fungal and bacterial immunity by inducing expression of proinflammatory cytokines, chemokines, and antimicrobial peptides (2). In addition, IL-17A contributes to the pathogenesis of several autoimmune diseases (3). IL-17E promotes Th2 cell responses (4). The roles of IL-17B, IL-17C, and IL-17D are less clear, however these family members also appear to have the capacity to induce proinflammatory cytokines (1,5,6). IL-17 receptors have an extracellular domain, a transmembrane domain, and a SEFIR domain. They are believed to signal as homodimers, heterodimers, or multimers through their SEFIR domain by recruiting the SEFIR domain-containing adaptor Act1 (7). Unlike most cytokines that signal through Jak/STAT pathways, IL-17 signaling results in NF-κB activation (8).IL-17A is a cysteine-linked, homodimeric, pro-inflammatory cytokine produced by Th17 cells, a distinct CD4+ T cell lineage (9,10). IL-17A stimulates the production of the pro-inflammatory cytokines IL-1β, TNFα, and IL-6. IL-17A also induces production of the neutrophil chemoattractants IL-8, CXCL1, and CXCL6 thereby bridging adaptive and innate immunity (9,10). IL-17A is intimately involved in mucosal immunity against bacterial infections (9,11) and has a putative role in some autoimmune disorders (9,12). IL-17A effects appear to be exerted primarily through binding to one of the IL-17 receptor subunits, IL-17RA (13). IL-17 binding induces production of cytokines, chemokines, and other proteins through activation of the Erk1/2 MAP kinase, PI3K/Akt, p38, and NF-κB pathways (11,12,14). Phosphorylation of some Jaks and Stats has been observed. 1.Gaffen, S.L. (2009) Nat Rev Immunol 9, 556-67. 2.Iwakura, Y. et al. (2011) Immunity 34, 149-62. 3.Hu, Y. et al. (2011) Ann N Y Acad Sci 1217, 60-76. 4.Fort, M.M. et al. (2001) Immunity 15, 985-95. 5.Yamaguchi, Y. et al. (2007) J Immunol 179, 7128-36. 6.Li, H. et al. (2000) Proc Natl Acad Sci U S A 97, 773-8. 7.Chang, S.H. et al. (2006) J Biol Chem 281, 35603-7. 8.Shalom-Barak, T. et al. (1998) J Biol Chem 273, 27467-73. 9.Kolls, J.K. and Lindén, A. (2004) Immunity 21, 467-76. 10.Liang, S.C. et al. (2006) J Exp Med 203, 2271-9. 11.Dubin, P.J. and Kolls, J.K. (2008) Immunol Rev 226, 160-71. 12.Zrioual, S. et al. (2009) J Immunol 182, 3112-20. 13.Wright, J.F. et al. (2008) J Immunol 181, 2799-805. 14.Rahman, M.S. et al. (2006) J Immunol 177, 4064-71.