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)|
|Recommended Dilution Buffer|
in vivo LFA-1 neutralization
|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 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.