InVivoMAb anti-human LFA-1α (CD11a)

Catalog #BE0005
Clone:
TS-1/22.1.1.13
Reactivities:
Human

$150.00 - $3,920.00

In stock
Only %1 left

Product Details

The TS-1/22.1.1.13 monoclonal antibody reacts with human LFA-1α(lymphocyte function-associated antigen 1 alpha) also known as integrin alpha L chain and CD11a. LFA-1αand CD18 combine to form LFA-1 a 180 kDa glycoprotein and a member of the integrin family. LFA-1 is expressed on the surface of all leukocytes including lymphocytes monocytes macrophages and granulocytes. LFA-1 plays a central role in leukocyte intercellular adhesion through interactions with its ligands ICAM-1 (CD54) ICAM-2 (CD102) and ICAM-3 (CD50) and also functions in lymphocyte costimulatory signaling.

Specifications

Isotype Mouse IgG1
Recommended Isotype Control(s) InVivoMAb mouse IgG1 isotype control, unknown specificity
Recommended Dilution Buffer InVivoPure pH 7.0 Dilution Buffer
Immunogen Human cytolytic T cells
Reported Applications in vitro LFA-1 neutralization
Formulation PBS, pH 7.0
Contains no stabilizers or preservatives
Endotoxin <2EU/mg (<0.002EU/μg)
Determined by LAL gel clotting assay
Purity >95%
Determined by SDS-PAGE
Sterility 0.2 μM filtered
Production Purified from tissue culture supernatant in an animal free facility
Purification Protein G
RRID AB_1107580
Molecular Weight 150 kDa
Storage The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.
in vitro LFA-1 neutralization
Kitchens, W. H., et al. (2012). "Combined costimulatory and leukocyte functional antigen-1 blockade prevents transplant rejection mediated by heterologous immune memory alloresponses" Transplantation 93(10): 997-1005. PubMed

BACKGROUND: Recent evidence suggests that alloreactive memory T cells are generated by the process of heterologous immunity, whereby memory T cells arising in response to pathogen infection crossreact with donor antigens. Because of their diminished requirements for costimulation during recall, these pathogen-elicited allocrossreactive memory T cells are of particular clinical importance, especially given the emergence of costimulatory blockade as a transplant immunosuppression strategy. METHODS: We used an established model of heterologous immunity involving sequential infection of a naive C57BL/6 recipient with lymphocytic choriomeningitis virus and vaccinia virus, followed by combined skin and bone marrow transplant from a BALB/c donor. RESULTS: We demonstrate that coupling the integrin antagonist anti-leukocyte functional antigen (LFA)-1 with costimulatory blockade could surmount the barrier posed by heterologous immunity in a fully allogeneic murine transplant system. The combined costimulatory and integrin blockade regimen suppressed proliferation of alloreactive memory T cells and attenuated their cytokine effector responses. This combined blockade regimen also promoted the retention of FoxP(3)(+) Tregs in draining lymph nodes. Finally, we show that in an in vitro mixed lymphocyte reaction system using human T cells, the combination of belatacept and anti-LFA-1 was able to suppress cytokine production by alloreactive memory T cells that was resistant to belatacept alone. CONCLUSIONS: As an antagonist against human LFA-1 exists and has been used clinically to treat psoriasis, these findings have significant translational potential for future clinical transplant trials.