Enhancement of antigen driven lymphocyte proliferation secondary to gp41-induced B7 expression on adherent monocytes

Michael A Kolber, Maria O. Saenz

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

HIV-1 viral proteins are known to have immune regulatory effects. The interplay between these molecules and the host immune cells is complex. In this study the immune regulatory effects of gp41 on lymphocyte proliferation were evaluated as a function of the state of the monocyte. It is shown that monocyte adherence to tissue culture plates prevents suppression of lymphocyte proliferation to recall antigen in the presence of gp41. In addition, gp41 can enhance proliferation to low concentrations of Casta antigen when PBL are permitted time to adhere. It is shown that these effects are in part mediated through enhanced expression of the costimulatory molecules B7 and CD40. Cyclosporin A was not able to fully abrogate gp41-enhanced proliferation, indicating participation of a calcium-independent pathway. In addition, concentrations of anti-IL2 receptor antibody sufficient to inhibit maximal proliferation to antigen did not fully inhibit PBL proliferation to antigen that is augmented with gp41. Taken together these results suggest that modification of the monocyte state of activation or differentiation could mediate a response to gp41 that is immune enhancing.

Original languageEnglish
Pages (from-to)35-44
Number of pages10
JournalCellular Immunology
Volume214
Issue number1
DOIs
StatePublished - Nov 25 2001

Fingerprint

Monocytes
Lymphocytes
Antigens
B7 Antigens
Interleukin-2 Receptors
Viral Proteins
Cyclosporine
HIV-1
Calcium
Antibodies

Keywords

  • Gp41
  • HIV/AIDS
  • Human PBL
  • Lymphocyte proliferation
  • Recall antigen

ASJC Scopus subject areas

  • Cell Biology
  • Immunology

Cite this

Enhancement of antigen driven lymphocyte proliferation secondary to gp41-induced B7 expression on adherent monocytes. / Kolber, Michael A; Saenz, Maria O.

In: Cellular Immunology, Vol. 214, No. 1, 25.11.2001, p. 35-44.

Research output: Contribution to journalArticle

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