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Monocytes in HIV type 1-infected individuals lose expression of costimulatory B7 molecules and acquire cytotoxic activity

Academic Article
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Overview

authors

  • Dudhane, A.
  • Conti, Bruno
  • Orlikowsky, T.
  • Wang, Z. Q.
  • Mangla, N.
  • Gupta, A.
  • Wormser, G. P.
  • Hoffmann, M. K.

publication date

  • 1996

journal

  • AIDS Research and Human Retroviruses  Journal

abstract

  • Monocytes/macrophages control the function of lymphocytes through positive and negative regulation. They release immunostimulatory cytokines and initiate costimulatory signals in T cells through the expression of B7 molecules. Their negative regulatory functions include the capacity to destroy cells with which they form cellular conjugates. We show here that HIV-1 infection skews monocyte function toward negative regulation by restraining the expression of costimulatory B7 molecules and by enhancing the cytolytic monocyte function. Monocytes that express constitutively B7, a membrane component that facilitates the engagement of costimulatory signals in T cells, lose this marker after HIV-1 infection and become refractory to inducers of B7 expression. The appearance of monocytes with reduced B7 expression is associated with an increased cytolytic monocyte capacity. Monocytes from HIV-1-infected donors destroy antibody-targeted normal lymphocytes more efficiently than do normal monocytes and they destroy CD4+ T cells specifically without the exposure to an exogenous ligand. CD4-reactive HIV-1 envelope molecules, expressed on monocytes as a consequence of infection or of opsonization by antibody, may specifically target CD4+ T lymphocytes for destruction and may thereby contribute to the preferential loss of CD4 T cells in HIV-1-infected individuals.

subject areas

  • Acquired Immunodeficiency Syndrome
  • Adult
  • Antigens, CD80
  • CD4-Positive T-Lymphocytes
  • Cells, Cultured
  • Child
  • Cytotoxicity, Immunologic
  • HIV-1
  • Humans
  • Monocytes
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Identity

International Standard Serial Number (ISSN)

  • 0889-2229

Digital Object Identifier (DOI)

  • 10.1089/aid.1996.12.885

PubMed ID

  • 8798973
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Additional Document Info

start page

  • 885

end page

  • 892

volume

  • 12

issue

  • 10

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