Mouse IL-27 R alpha/WSX-1/TCCR PE-conjugated Antibody

IL-27 R alpha, also known as WSX-1 and TCCR, is a 85‑95 kDa member of the type I, group 2 cytokine receptor family (1-6). Mature IL-27 R alpha is a type I transmembrane glycoprotein that contains a 486 amino acid (aa) extracellular region, a 21 aa transmembrane segment and a 92 aa cytoplasmic domain. Consistent with type I cytokine receptors, the extracellular region contains four positionally conserved cysteine residues, a WSxWS motif (for receptor folding and ligand binding), and three fibronectin type III repeats. The intracellular domain contains a “box-1” motif that may be involved with Janus kinases (3). In mouse, a soluble 33 kDa splice form that shows a 20 aa substitution for aa 251-623 has been identified (7). The mouse IL-27 R alpha extracellular region shares 63% amino acid identity with the human IL-27 R alpha extracellular domain (2, 3). IL-27 R alpha is expressed in mast cells, endothelial cells, NK cells, macrophages, monocytes, B cells, dendritic cells, and naïve T cells (1, 2, 4, 8). Typical of other class I cytokine receptor chains, the ligand binding IL-27 R alpha molecule is known to heterodimerize with a signal-transducing subunit (gp130) to form a functional IL-27 receptor (9, 10). In addition, IL-27 R alpha is reported to complex with CNTFR alpha and gp130 form a humanin receptor on neurons (7, 11), and to complex with gp130 and IL-6 R to form a receptor for a p28:CLF heterodimeric cytokine on lymphocytes (12). Studies using IL-27 R alpha/WSX-1^-/- mice reveal that IL-27 has the ability to suppress T cell activity during infection, and to mediate an inhibition of both type 1 and type 2 T cell immunity (4, 13, 14). In particular, IL-27 is known to act on naïve T cells, blocking their differentiation into a Th17 phenotype. Notably, cells committed to a Th17 phenotype, although they express a functional IL-27 receptor, are unresponsive to the effects of IL-27 (15). Activated T cells that are CD4+ and CD8+, and which express the IL-27 receptor, can be induced by IL‑27 to form a double-positive CD25⁺ FoxP3^- IFN-gamma plus IL-10 secreting phenotype that both promotes and suppresses the inflammatory response (16).