Human IL-13 R alpha 2 Antibody

Applications

Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.

Preparation and Storage

Background: IL-13 R alpha 2

Interleukin‑13 Receptor alpha 2 (IL‑13 R alpha 2), also known as IL‑13 binding protein, and CD213a2, is a widely expressed 55 kDa cytokine receptor that plays an important role in the Th2‑polarized immune responses characteristic of a variety of pathologies, including parasitic infections and allergic asthma (1, 2). Mature human IL‑13 R alpha 2 consists of a 317 amino acid (aa) extracellular domain with three fibronectin type‑III domains, a WSxWS motif, a 20 aa transmembrane segment, and a 17 aa cytoplasmic domain (3). Within the ECD, human IL‑13 R alpha 2 shares 64% and 62% aa sequence identity with mouse and rat IL‑13 R alpha 2, respectively. In both mouse and human, a 40 kDa‑50 kDa soluble form of IL‑13 R alpha 2 can be generated by MMP‑8 mediated shedding in vitro (4).  Although this is assumed to occur in vivo in mouse, there is no evidence that shedding occurs in human (5‑7).  In mouse, alternative splicing also leads to sIL‑13 R alpha 2, but again, this phenomenon apparently does not occur in human (6‑7).  Thus, the biological effects of human IL‑13 R alpha 2 would appear to be mediated exclusively by membrane IL‑13 R alpha 2 (7). The biological effects of IL‑13 and IL‑4 are closely related in part due to a shared receptor system. IL‑13 binds to IL‑13 R alpha 1 which then forms a signaling complex with IL‑4 R alpha (8, 9). IL‑13 R alpha 2 functions as a decoy receptor by binding and internalizing IL‑13 and preventing it from signaling through the IL‑13 R alpha 1/IL‑4 R alpha complex (3, 10). IL‑13 R alpha 2 can also block IL‑4 induced responses by inhibiting IL‑4 bound IL‑13 R alpha 1/IL‑4 R alpha receptor complexes even though it does not itself bind IL‑4 (11, 12). Aside from its decoy function, IL‑13‑activated IL‑13 R alpha 2 directly promotes the development of tissue fibrosis by inducing the transcription of TGF‑ beta (13). Presumably, any human soluble IL‑13 R alpha 2, if it exists, will retain its ligand binding capability and attenuate responses to IL‑13 but not to IL‑4 (11, 14). The up‑regulation of transmembrane during Th2‑biased immune responses limits the extent of those responses (15‑17).

Product Datasheets

Related Research Areas

• Cytokines and Receptors in Allergy and Asthma
• Cytokines and Receptors in Angiogenesis
• Cytokines and Receptors in Tfh Cell Differentiation and Function