MIP-1α Induces Binding of Nuclear Factors to the κB DNA Element in Human B Cells

Abstract

The chemokine macrophage inflammatory protein-1 alpha (MIP-1α) stimulates migration of B cells through an unknown mechanism. Furthermore, little is known about signal transduction mechanisms through which MIP-1α might signal phenotypic changes in B cells. We are investigating the role of MIP-1α in B cell signaling. Here we report that stimulation of the Ramos B cell line or tonsil B or peripheral blood-B (PBL-B) cells with MIP-1α caused the transcription factor NF-κB to bind to DNA. NF-κB induction was dose dependent, and was transient, with peak induction occurring at 30 min. MIP-1α treatment stimulated the degradation of IκBα, a cytoplasmic inhibitor of NF-κB. The biological significance of NF-κB activation by MIP-1α is currently unknown, but it is known that NF-κB modulates expression of genes involved in many inflammatory and immune responses. Here we show that NF-κB activation is a target of signals sent into B cells by MIP-1α.