NF-κB Activation for Constitutive Expression of VCAM-1 and ICAM-1 on B Lymphocytes and Plasma Cells

Abstract

Cytokine stimulation can activate NF-κB that triggers inducible expression of E-selectin, VCAM-1 (Vascular Cell Adhesion Molecule-1) and ICAM-1 (Intercellular Cell Adhesion Molecule-1) in endothelial cells. In the previous study, we have shown that B lymphocytes and plasma cells can express E-selectin by constitutive activation of NF-κB. Here we show that human B lymphocytes and ARH-77 plasma cells expressed VCAM-1 and ICAM-1 in a cytokine dispensable mechanism. NF-κB antagonists could inhibit their expressions in ARH-77 cells. The activities of NF-κB for VCAM-1 and ICAM-1 promoters prior to cytokine stimulation were detected in ARH-77 cells using electrophoretic mobility shift assays. Again, NF-κB antagonists could abrogate these promoter activities. Taken together, our results demonstrate that NF-κB activation is the underlying molecular mechanism for constitutive expression of E-selectin, VCAM-1, and ICAM-1 on human B lymphocytes and plasma cells.