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Presentation of exogenous whole inactivated simian immunodeficiency virus by mature dendritic cells induces CD4(+) and CD8(+) T-Cell responses

  1. Author:
    Frank, I.
    Santos, J. J.
    Mehlhop, E.
    Villamide-Herrera, L.
    Santisteban, C.
    Gettie, A.
    Ignatius, R.
    Lifson, J. D.
    Pope, M.

  2. Author Address

    Populat Council, Ctr Biomed Res, 1230 York Ave, New York, NY 10021 USA Populat Council, Ctr Biomed Res, New York, NY 10021 USA Aaron Diamond AIDS Res Ctr, New York, NY USA Free Univ Berlin, Benjamin Franklin Med Ctr, Dept Med Microbiol & Immunol Infect, D-1000 Berlin, Germany NCI, Retroviral Pathogenesis Lab, AIDS Vaccine Program, SAIC Frederick, Frederick, MD 21701 USA Pope M Populat Council, Ctr Biomed Res, 1230 York Ave, New York, NY 10021 USA
    1. Year: 2003
  2. Journal: Jaids-Journal of Acquired Immune Deficiency Syndromes
    1. 34
    2. 1
    3. Pages: 7-19
  4. Type of Article: Article
  1. Abstract:

    Interactions between HIV-1 and dendritic cells (DCs) play an important role in the initial establishment and spread of infection and development of antiviral immunity. We used chemically inactivated aldrithiol-2 (AT-2) simian immunodeficiency virus (SIV) with functional envelope glycoproteins to study virus interactions with DCs and developed an in vitro system to evaluate the quality of SIV antigen (Ag) presentation by DCs to T cells. AT-2 SIV interacts authentically with T cells and DCs and thus allows assessment of natural SIV-specific responses. CD4(+) and CD8(+) T cells from blood or lymph nodes of SIV-infected macaques released interferon-gamma (IFNgamma) and proliferated in response to a variety of AT-2 SIV isolates. Responses did not vary significantly as a function of the quantitative envelope glycoprotein content of the virions. Presentation of Ags derived from AT-2 SIV by DCs was more potent than presentation by comparably Ag-loaded monocytes. Interestingly, SIV-pulsed mature DCs stimulated both CD4(+) and CD8(+) T-cell responses, whereas immature DCs primarily stimulated CD4(+) T cells. Further studies using AT-2 inactivated virus may help to define better the details of the virus-DC interactions critical for infection versus induction of antiviral immune responses.

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