IL-17A (D1X7L) Rabbit mAb (BSA and Azide Free) #90428

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.