Modulation of macrophage inflammatory protein-1alpha and its receptors in human B-cell lines derived from patients with acquired immunodeficiency syndrome and Burkitt's lymphoma.

Macrophage inflammatory protein-1 alpha (MIP-1alpha) is a member of the -C-C- family of low-molecular weight chemokines. MIP-1alpha is involved in the homeostatic control of stem cell proliferation, in inducing chemotaxis, and also in inflammatory responses in mature cell types. In order to observe modulations of MIP-1alpha secretion and expression along with MIP-1alpha receptor (MIP-1alpha-R) expression for a possible autocrine role in AIDS associated B-cell lines, we studied a wide panel of human B-cell lines. Previous work by us has shown that HIV-1 tat down modulates MIP-1alpha by inducing a novel transcription factor MNP. Our data in this report suggest that HIV down modulates MIP-1alpha as a mechanism to evade suppression by this chemokine in human B-cells. Furthermore, our results strongly suggest MIP-1alpha autocrine loops in a majority of tumor B-cells as evident by MIP-1alpha-R expression, and also secretion of MIP-1alpha.