Journal Article

Phosphoantigen-Reactive Vγ9Vδ2 T Lymphocytes Suppress In Vitro Human Immunodeficiency Virus Type 1 Replication by Cell-Released Antiviral Factors Including CC Chemokines

Fabrizio Poccia, Luca Battistini, Barbara Cipriani, Giorgio Mancino, Federico Martini, Marie Lise Gougeon and Vittorio Colizzi

in The Journal of Infectious Diseases

Published on behalf of Infectious Diseases Society of America

Volume 180, issue 3, pages 858-861
Published in print September 1999 | ISSN: 0022-1899
Published online September 1999 | e-ISSN: 1537-6613 | DOI: https://dx.doi.org/10.1086/314925
Phosphoantigen-Reactive Vγ9Vδ2 T Lymphocytes Suppress In Vitro Human Immunodeficiency Virus Type 1 Replication by Cell-Released Antiviral Factors Including CC Chemokines

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Vγ9Vδ2 T lymphocytes are broadly reactive against various intracellular pathogens and display both lytic and proliferative responses to human immunodeficiency virus (HIV)-infected cells. HIV infection of peripheral blood mononuclear cell cultures led to absolute increases in Vγ9Vδ2 T cells accompanied by decreased p24 levels. Strong γδ T cell activation with nonpeptidic mycobacterial phosphoantigens (TUBAg1 extract or synthetic isopentenyl pyrophosphate) resulted in potent inhibition of HIV replication through soluble released factors. Subsequent analyses showed that phosphoantigen-activated γδ T cells produced substantial amounts of b-chemokines (macrophage inflammatory protein [MIP]-1α, MIP-1β, and regulated-on-activation, normal T-cell—expressed and -secreted beta-chemokine [RANTES]), which represent the natural ligand for the CCR5 HIV coreceptor. Accordingly, anti-β-chemokine antibodies neutralized the inhibition of monocytotropic HIV strains by γδ T cell-released factors. Moreover, a T-tropic HIV strain using the CXCR4 coreceptor for virus entry was potently inhibited. Together, these data reveal that phosphoantigen-activated γδ T cells are an important source of CC chemokines and may suppress HIV replication through cell-released antiviral factors.

Journal Article.  2585 words.  Illustrated.

Subjects: Infectious Diseases ; Immunology ; Public Health and Epidemiology ; Microbiology

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