CD50/ICAM-3 ELISA Kit

Migration of CD4-positive lymphocytes into the vessel wall is a critical step in atherogenesis. Recent data suggest that CD4-positive lymphocytes express the nuclear transcription factors Liver-X-Receptor (LXR) alpha and beta with an effect of LXR activators on TH1-cytokine release from these cells. However, the role of LXR in lymphocyte migration remains currently unexplored. Therefore, the present study investigated whether LXR activation might modulate chemokine-induced migration of these cells. Stimulation of CD4-positive lymphocytes with SDF-1 leads to a 2.5 +/- A 0.8-fold increase in cell migration (P < 0.05; n = 12). Pretreatment of cells with the LXR activator T0901317 reduces this effect in a concentration-dependent manner to a maximal 0.9 +/- A 0.4-fold induction at 1 mu mol/L T0901317 (P < 0.05 compared to SDF-1-treated cells; n = 12). Similar results were obtained with the LXR activator GW3965. The effect of LXR activators on CD4-positive lymphocyte migration was mediated through an early inhibition of chemokine-induced PI-3 kinase activity as determined by PI-3 kinase activity assays. Downstream, T0901317 inhibited activation of the small GTPase Rac and phosphorylation of the myosin light chain (MLC). Moreover, LXR activator treatment reduced f-actin formation as well as ICAM3 translocation to the uropod of the cell, thus interfering with two important steps in T cell migration. Transfection of CD4-positive lymphocytes with LXR alpha/beta siRNA abolished T0901317 inhibitory effect on MLC phosphorylation and ICAM3 translocation. LXR activation by T0901317 or GW3965 inhibits chemokine-induced migration of CD4-positive lymphocytes. Given the crucial importance of chemokine-induced T cell migration in early atherogenesis, LXR activators may be promising tools to modulate this effect.

Cell adhesion molecules play an important role during immune responses, Circulating (c) forms of these molecules Rave been used as monitors of disease progression. In this study, we have investigated serum levels of ICAM1, ICAM2, ICAM3 and VCAM1 in HIV-infected patients. Our results showed that levels of cICAMs and cVCAM1 are increased during HIV infection. Among an HIV-infected population, the cICAM2 level was higher in the asymptomatic group compared to the AIDS group. In contrast, the cICAM1 level was higher in the AIDS group compared to the asymptomatic group. No difference between the two groups was observed in cICAM3 and cVCAM1 levels. A significant correlation was found between cICAM1, cICAM2 and cVCAM1 in both populations. We also showed that the cICAM1/cICAM2 ratio was correlated with the increase in the cp, microglobulin level and the decrease in CD4 T-cell counts in the AIDS group. These results indicate that serum cCAM1 and cICAM2 in HIV infection could be additional markers to discriminate between asymptomatic and progressor patients.