InVivoMAb anti-mouse IL-21R

Clone Catalog # Category
4A9 BE0258 InVivoMab Antibodies
$95 - $3250

About InVivoMAb anti-mouse IL-21R

The 4A9 monoclonal antibody reacts with mouse IL-21 receptor (IL-21 R) also known as CD360. IL-21 R is a member of the type 1 cytokine receptor family that forms a functional heterodimeric receptor complex with the common gamma chain (CD132). IL-21 R is expressed on both resting and activated B cells, T cells, NK cells and dendritic cells. Upon IL-21 binding, IL-21 R activates downstream Jak-1, Jak-3, STAT1, STAT3 and STAT 5 signal transduction pathways to induce the proliferation and differentiation of T lymphocytes, B lymphocytes, and NK cells. The 4A9 antibody has been shown to block the biological activity of IL-21 R in vivo.

InVivoMAb anti-mouse IL-21R Specifications

Isotype

Rat IgG2a, κ

Recommended Isotype Control(s) InVivoMAb rat IgG2a isotype control, anti-trinitrophenol(BE0089)
Recommended InVivoPure Dilution Buffer InVivoPure pH 7.0 Dilution Buffer(IP0070)
Immunogen

Rat YB2/0 cell line expressing truncated IL-21 R

Reported Applications

in vivo IL-21R blockade

Endotoxin
  • <2EU/mg (<0.002EU/μg)
  • Determined by LAL gel clotting assay
Purity
  • >95%
  • Determined by SDS-PAGE
Formulation
  • PBS, pH 7.0
  • Contains no stabilizers or preservatives
Sterility

0.2 μM filtered

Production

Purified from tissue culture supernatant in an animal free facility

Purification

Protein G

Storage

The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.

RRID

AB_2687737

Molecular Weight

150 kDa

Application References

InVivoMAb anti-mouse IL-21R (Clone: 4A9)

  Clemente-Casares, X., et al. (2016). "Expanding antigen-specific regulatory networks to treat autoimmunity." Nature 530(7591): 434-440. PubMed

Regulatory T cells hold promise as targets for therapeutic intervention in autoimmunity, but approaches capable of expanding antigen-specific regulatory T cells in vivo are currently not available. Here we show that systemic delivery of nanoparticles coated with autoimmune-disease-relevant peptides bound to major histocompatibility complex class II (pMHCII) molecules triggers the generation and expansion of antigen-specific regulatory CD4(+) T cell type 1 (TR1)-like cells in different mouse models, including mice humanized with lymphocytes from patients, leading to resolution of established autoimmune phenomena. Ten pMHCII-based nanomedicines show similar biological effects, regardless of genetic background, prevalence of the cognate T-cell population or MHC restriction. These nanomedicines promote the differentiation of disease-primed autoreactive T cells into TR1-like cells, which in turn suppress autoantigen-loaded antigen-presenting cells and drive the differentiation of cognate B cells into disease-suppressing regulatory B cells, without compromising systemic immunity. pMHCII-based nanomedicines thus represent a new class of drugs, potentially useful for treating a broad spectrum of autoimmune conditions in a disease-specific manner.

Cao, A. T., et al. (2015). "Interleukin (IL)-21 promotes intestinal IgA response to microbiota." Mucosal Immunol 8(5): 1072-1082. PubMed

Commensal microbiota-specific T helper type 17 (Th17) cells are enriched in the intestines, which can convert into T follicular helper (Tfh) in Peyer's patches, and are crucial for production of intestinal immunoglobulin A (IgA) against microbiota; however, the role of Th17 and Tfh cytokines in regulating the mucosal IgA response to enteric microbiota is still not completely known. In this study, we found that intestinal IgA was impaired in mice deficient in interleukin (IL)-17 or IL-21 signaling. IL-21, but not IL-17, is able to augment B-cell differentiation to IgA(+) cells as mediated by transforming growth factor beta1 (TGFbeta1) and accelerate IgA class switch recombination (CSR). IL-21 and retinoic acid (RA) induce IgA(+) B-cell development and IgA production and drives autocrine TGFbeta1 production to initiate IgA CSR. Repletion of T-cell-deficient TCRbetaxdelta(-/-) mice with Th17 cells specific for commensal bacterial antigen increased the levels of IgA(+) B cells and IgA production in the intestine, which was blocked by neutralizing IL-21. Thus IL-21 functions to strongly augment IgA production under intestinal environment. Furthermore, IL-21 promotes intestinal B-cell homing through alpha4beta7 expression, alone or with TGFbeta and RA. Together, IL-21 from microbiota-specific Th17 and/or Tfh cells contributes to robust intestinal IgA levels by enhancing IgA(+) CSR, IgA production and B-cell trafficking into the intestine.

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