About InVivoMAb anti-mouse TCRβ
The H57-597 monoclonal antibody reacts with the beta chain of the mouse T cell receptor (TCR). TCRβ belongs to the immunoglobulin superfamily and is expressed by thymocytes and T lymphocytes. TCRβ combines with TCRα to form TCR α/β. TCR α/β plays a central role in antigen recognition, signal transduction, and T cell activation. The H57-597 antibody has been shown to deplete TCR α/β bearing T cells following in vivo administration.
InVivoMAb anti-mouse TCRβ Specifications
|Isotype||Armenian Hamster IgG|
|Recommended Isotype Control(s)|
|Recommended Dilution Buffer|
|Immunogen||Affinity purified TCR from mouse DO-11.10 cells|
in vivo T cell depletion
|Sterility||0.2 μM filtered|
|Production||Purified from tissue culture supernatant in an animal free facility|
|Molecular Weight||150 kDa|
|Storage||The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.|
InVivoMAb anti-mouse TCRβ (Clone: H57-597 (HB218))
Schroder, P. M., et al. (2013). “Transient combination therapy targeting the immune synapse abrogates T cell responses and prolongs allograft survival in mice.” PLoS One 8(7): e69397. PubMed
T cells play a major role in allograft rejection, which occurs after T cell activation by the engagement of several functional molecules to form an immune synapse with alloantigen presenting cells. In this study, the immune synapse was targeted using mAbs directed to the TCR beta-chain (TCRbeta) and lymphocyte function-associated antigen-1 (LFA1) to induce long-term allograft survival. Evaluation of antigen-specific T cell responses was performed by adoptively transferring CFSE labeled transgenic OT-II cells into wild-type mice and providing OVA peptide by intravenous injection. Graft survival studies were performed in mice by transplanting BALB/c ear skins onto the flanks of C57BL/6 recipients. The anti-TCRbeta plus anti-LFA1 mAb combination (but not either mAb alone) abrogated antigen-specific T cell responses invitro and invivo. Transient combination therapy with these agents resulted in significantly prolonged skin allograft survival in mice (51+/-10 days; p<0.01) when compared to treatment with either anti-TCRbeta mAb (24+/-5 days) or anti-LFA1 mAb (19+/-3 days) alone or no treatment (10+/-1 days). When lymphoid tissues from these mice were analyzed at different times post-transplant, only those receiving the combination of anti-TCRbeta and anti-LFA1 mAbs demonstrated long-lasting reductions in total T cell numbers, cellular and humoral anti-donor responses, and expression of CD3 on the surface of T cells. These results demonstrate that transient anti-TCRbeta and anti-LFA1 mAb combination therapy abrogates antigen-reactive T cell responses with long-lasting effects that significantly prolong allograft survival.
Gillard, G. O., et al. (2011). “Thy1+ NK cells from vaccinia virus-primed mice confer protection against vaccinia virus challenge in the absence of adaptive lymphocytes.” PLoS Pathog 7(8): e1002141. PubMed
While immunological memory has long been considered the province of T- and B-lymphocytes, it has recently been reported that innate cell populations are capable of mediating memory responses. We now show that an innate memory immune response is generated in mice following infection with vaccinia virus, a poxvirus for which no cognate germline-encoded receptor has been identified. This immune response results in viral clearance in the absence of classical adaptive T and B lymphocyte populations, and is mediated by a Thy1(+) subset of natural killer (NK) cells. We demonstrate that immune protection against infection from a lethal dose of virus can be adoptively transferred with memory hepatic Thy1(+) NK cells that were primed with live virus. Our results also indicate that, like classical immunological memory, stronger innate memory responses form in response to priming with live virus than a highly attenuated vector. These results demonstrate that a defined innate memory cell population alone can provide host protection against a lethal systemic infection through viral clearance.