Anti-CD84 monoclonal antibody, clone FQS9435 [Alexa Fluor® 488]

Trichloroethylene (ICE) is suspected as a potent immunomodulator that accelerates the development of allergic diseases. We previously reported that TCE promotes ovalbumin (OVA)-induced active cutaneous anaphylaxis, including enhancing antigen-specific serum IgE levels and splenic lymphocyte proliferation. However, the target cells and molecular mechanism through which TCE modulates antigen-specific immune responses remain unclear. To identify a potential underlying mechanism, we investigated whether TCE modulates T cell receptor (TCR)-induced T cell activation and proliferation in vitro. TCE enhanced T cell proliferation primed by anti-CD3 antibody, but not concanavalin A, in a dose-dependent fashion. In addition, TCE enhanced anti-CD3-primed proliferation of CD8(+) rather than CD4(+) T cells. Consistent with this result, TCE markedly enhanced the Lck phosphorylation mediated by anti-CD3 antibody in CD8(+) but not CD4(+) T cells. Furthermore, we analyzed the effect of TCE exposure via drinking water for 2 weeks on splenocyte populations in non-immunized and OVA-immunized mice. In OVA-immunized mice, TCE (3 mg/l) significantly expanded CD3(+), CD8(+) and CD4(+) cell populations, however the effect at the lower concentration was significant only in the CD8(+) populations, whereas TCE had no effect on these cells population in non-immunized mice. These findings suggest that TCE enhances TCR-CD3-induced proliferation of CD8(+) rather than CD4(+) cells and disrupts various activities of peripheral T cells.

The CD2-subset of the immunoglobulin superfamily of cell surface receptors is an emerging family of proteins involved in cellular activation. Members of this family are CD2, CD48, CD58, CD84, signaling lymphocytic activation molecule (SLAM), 2B4 and Ly-9. These proteins are expressed on different leukocyte populations and the receptors of this family, specifically CD2, 2B4 and SLAM, contribute to the activation of T cells and natural killer cells. 2B4 and SLAM associate with a protein termed SLAM-associated protein that is the genetic defect in the immunodeficiency X-linked lymphoproliferative syndrome. Impaired signaling via these receptors may contribute to this often-fatal immunodeficiency.