Cutting Edge: HIV-1 Tat Protein Differentially Modulates the B Cell Response of Naive, Memory, and Germinal Center B Cells

Critical steps of B cell differentiation occur within lymphoid organs that are also major sites of HIV-1 replication. Because Tat can be released by infected cells, we investigated whether extracellular HIV-1 Tat modulates cell proliferation of B cells at critical stages of their differentiation. He...

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Bibliographic Details
Published in:The Journal of immunology (1950) 1999-08, Vol.163 (3), p.1119-1122
Main Authors: Lefevre, Eric A, Krzysiek, Roman, Loret, Erwann P, Galanaud, Pierre, Richard, Yolande
Format: Article
Language:English
Subjects:
Adjuvants, Immunologic - pharmacology
Adjuvants, Immunologic - physiology
AIDS/HIV
Antibodies, Anti-Idiotypic - pharmacology
Antibodies, Monoclonal - pharmacology
B-Lymphocyte Subsets - cytology
B-Lymphocyte Subsets - immunology
CD40 Antigens - immunology
Cell Division - immunology
Cells, Cultured
Child
Dose-Response Relationship, Immunologic
Gene Products, tat - pharmacology
Gene Products, tat - physiology
Germinal Center - cytology
Germinal Center - immunology
Growth Inhibitors - pharmacology
HIV-1 - immunology
Humans
Immune Sera - pharmacology
Immunoglobulin M - immunology
Immunologic Memory
Immunosuppressive Agents - pharmacology
Interleukin-4 - pharmacology
Interphase - immunology
Lymphocyte Activation - immunology
Palatine Tonsil
tat Gene Products, Human Immunodeficiency Virus
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Summary:Critical steps of B cell differentiation occur within lymphoid organs that are also major sites of HIV-1 replication. Because Tat can be released by infected cells, we investigated whether extracellular HIV-1 Tat modulates cell proliferation of B cells at critical stages of their differentiation. Here we show that extracellular Tat inhibited the proliferation of B cell receptor-triggered naive and memory B cells by >80% but had no effect on their CD40 mAb and IL-4-mediated proliferation. In striking contrast, Tat doubled the germinal center B cell proliferation induced by CD40 mAb and IL-4. These effects were dose dependent and required the addition of Tat at the initiation of the culture, suggesting that Tat acts on early stages of cell cycle progression. By its effects on B cell subsets, Tat might directly affect the normal B cell differentiation process in HIV-positive patients and favor the occurrence of AIDS-associated B cell lymphomas.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.163.3.1119