InVivoMAb rat IgG1 Isotype control, anti-trinitrophenol

Clone Catalog # Category
TNP6A7 BE0290 Isotype Controls
$95 - $3250

About InVivoMAb rat IgG1 Isotype control, anti-trinitrophenol

The TNP6A7 monoclonal antibody reacts with trinitrophenol (TNP). Because TNP is not expressed by mammals this antibody is ideal for use as an isotype-matched control for rat IgG1 antibodies in most in vivo and in vitro applications. This antibody can be used as an alternative to BE0088.

InVivoMAb rat IgG1 Isotype control, anti-trinitrophenol Specifications

Isotype

Rat IgG1, λ

Recommended InVivoPure Dilution Buffer InVivoPure pH 7.0 Dilution Buffer(IP0070)
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_2687813

RRID

AB_2687813

Molecular Weight

150 kDa

Application References

InVivoMAb rat IgG1 isotype control, anti-trinitrophenol (Clone: TNP6A7)

Bauche, D., et al. (2018). "LAG3(+) Regulatory T Cells Restrain Interleukin-23-Producing CX3CR1(+) Gut-Resident Macrophages during Group 3 Innate Lymphoid Cell-Driven Colitis." Immunity 49(2): 342-352 e345. PubMed Interleukin-22 (IL-22)-producing group 3 innate lymphoid cells (ILC3) maintains gut homeostasis but can also promote inflammatory bowel disease (IBD). The regulation of ILC3-dependent colitis remains to be elucidated. Here we show that Foxp3(+) regulatory T cells (Treg cells) prevented ILC3-mediated colitis in an IL-10-independent manner. Treg cells inhibited IL-23 and IL-1beta production from intestinal-resident CX3CR1(+) macrophages but not CD103(+) dendritic cells. Moreover, Treg cells restrained ILC3 production of IL-22 through suppression of CX3CR1(+) macrophage production of IL-23 and IL-1beta. This suppression was contact dependent and was mediated by latent activation gene-3 (LAG-3)-an immune checkpoint receptor-expressed on Treg cells. Engagement of LAG-3 on MHC class II drove profound immunosuppression of CX3CR1(+) tissue-resident macrophages. Our study reveals that the health of the intestinal mucosa is maintained by an axis driven by Treg cells communication with resident macrophages that withhold inflammatory stimuli required for ILC3 function.

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