InVivoMAb anti-human LFA-1α (CD11a)

CloneCatalog #Category
TS-1/22.1.1.13BE0005InVivoMab Antibodies
$95 - $3250

About InVivoMAb anti-human LFA-1α (CD11a)

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.

InVivoMAb anti-human LFA-1α (CD11a) Specifications

Isotype Mouse IgG1
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.

Application References

InVivoMAb anti-human LFA-1α (CD11a) (Clone: TS-1/22.1.1.13)

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.