About InVivoPlus 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 BP0088.
InVivoPlus rat IgG1 isotype control, anti-trinitrophenol Specifications
|Isotype||Rat IgG1, λ|
|Recommended Dilution Buffer|
|Sterility||0.2 μM filtered|
|Production||Purified from tissue culture supernatant in an animal free facility|
|Molecular Weight||150 kDa|
|*Murine Pathogen Test Results|
|Storage||The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.|
InVivoPlus 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.