InVivoMAb anti-mouse CD18

Clone Catalog # Category
M18/2 BE0009 InVivoMab Antibodies
$95 - $3250

About InVivoMAb anti-mouse CD18

The M18/2 monoclonal antibody reacts with mouse CD18, a 90-95 kDa type I transmembrane protein also known as integrin beta 2. CD18 combines with CD11a to form the integrin LFA-1 and combines with CD11b to form the integrin Mac-1. CD18 plays roles in cell adhesion as well as cell-surface mediated signaling.

InVivoMAb anti-mouse CD18 Specifications

Isotype

Rat IgG2a, κ

Recommended Isotype Control(s) InVivoMAb rat IgG2a isotype control, anti-trinitrophenol(BE0089)
Recommended InVivoPure Dilution Buffer InVivoPure pH 7.0 Dilution Buffer(IP0070)
Immunogen

C57BL/10 splenocytes

Reported Applications

in vivo LFA-1 neutralization

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 undiluted at 4°C, and protected from prolonged exposure to light. Do not freeze.

RRID

AB_1107607

Molecular Weight

150 kDa

Application References

InVivoMAb anti-mouse CD18 (Clone: M18/2)

Zumwalde, N. A., et al. (2013). "ICAM-1-dependent homotypic aggregates regulate CD8 T cell effector function and differentiation during T cell activation." J Immunol 191(7): 3681-3693. PubMed

A hallmark of T cell activation in vitro and in vivo is the clustering of T cells with each other via interaction of the LFA-1 integrin with ICAM-1. The functional significance of these homotypic aggregates in regulating T cell function remains unknown. We used an APC-free in vitro activation system to demonstrate that stimulation of purified naive CD8 T cells results in enhanced expression of ICAM-1 on T cells that is sustained by the inflammatory cytokine IL-12 and associated with robust T cell aggregates. ICAM-1-deficient CD8 T cells proliferate normally but demonstrate a striking failure to aggregate. Interestingly, loss of ICAM-1 expression results in elevated levels of IFN-gamma and granzyme B, as well as enhanced cytotoxicity. Similar results were obtained when anti-LFA-1 Ab was used to block the clustering of wild-type T cells. ICAM-1 ligation is not required for IFN-gamma regulation, as clustering of ICAM-1-deficient CD8 T cells with wild-type T cells reduces IFN-gamma expression. Analysis using a fluorescent reporter that monitors TCR signal strength indicates that T cell clustering limits T cell exposure to Ag during activation. Furthermore, T cell clustering promotes the upregulation of the CTLA-4 inhibitory receptor and the downregulation of eomesodermin, which controls effector molecule expression. Activation of ICAM-1-deficient CD8 T cells in vivo results in an enhanced percentage of KLRG-1(+) T cells indicative of short-lived effectors. These results suggest that T cell clustering represents a mechanism that allows continued proliferation but regulates T cell effector function and differentiation.

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