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(American Journal of Pathology. 2000;156:1441-1453.)
© 2000 American Society for Investigative Pathology

Regular Articles

Chemokine and Chemokine-Receptor Expression in Human Glial Elements

Induction by the HIV Protein, Tat, and Chemokine Autoregulation

Carrie M. McManus^*, Karen Weidenheim^*, Scott E. Woodman^*, Jeranil Nunez^*, Joseph Hesselgesser, Avindra Nath and Joan W. Berman^*§

From the Departments of Pathology^*
and Microbiology and Immunology,^§
Albert Einstein College of Medicine, Bronx, New York; the Department of Immunology,
Berlex Biosciences, Richmond, California; and the Departments of Neurology and Microbiology and Immunology,
Kentucky Clinic L445, University of Kentucky, Lexington, Kentucky

Human immunodeficiency virus (HIV) encephalitis is a prominent pathology seen in children infected with HIV. Immunohistochemical analyses of pediatric brain tissue showed distinct differences in expression of C-C chemokines and their receptors between children with HIV encephalitis and those with non-CNS-related pathologies. Evidence suggests that soluble factors such as HIV Tat released from HIV-infected cells may have pathogenic effects. Our results show Tat effects on chemokines and their receptors in microglia and astrocytes as well as chemokine autoregulation in these cells. These results provide evidence for the complex interplay of Tat, chemokines, and chemokine receptors in the inflammatory processes of HIV encephalitis and illustrate an important new role for chemokines as autocrine regulators.

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