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Related Experiment Videos

Complement activation by recombinant HIV-1 glycoprotein gp120

C Süsal1, M Kirschfink, M Kröpelin

  • 1Department of Transplantation Immunology, University of Heidelberg, Germany.

Journal of Immunology (Baltimore, Md. : 1950)
|June 15, 1994
PubMed
Summary

HIV-1 envelope glycoprotein gp120 can activate the complement system on CD4+ T cells, potentially explaining non-infected cell depletion in HIV patients. This complement activation occurs without antibodies, primarily through the classical pathway.

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Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • CD4+ T cell depletion is a hallmark of HIV infection, but its mechanisms remain unclear.
  • The role of complement system activation in HIV pathogenesis requires further investigation.

Purpose of the Study:

  • To determine if HIV-1 envelope glycoprotein gp120 can activate the complement system independently of anti-gp120 antibodies.
  • To elucidate the pathway of complement activation by gp120 and its potential role in CD4+ T cell loss.

Main Methods:

  • Incubation of gp120-coated CD4+ T cells with autologous serum from healthy individuals.
  • Assessment of complement protein binding (C4, C3d, C5b-9, properdin) using immunofluorescence.
  • Complement activation pathway analysis using sera deficient in complement components (C1q, C4) and EDTA.

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  • Lymphocytotoxicity assays using human and rabbit sera to evaluate cell lysis.

    • Main Results:

    • Complement proteins C4, C3d, C5b-9, and properdin bound to gp120-coated CD4+ T cells in autologous serum.
    • Complement activation occurred mainly via the classical pathway, dependent on C1q and C4, and inhibited by EDTA.
    • No significant lysis of gp120-coated cells was observed with human serum, but rabbit serum induced lysis due to natural IgM antibodies.
    • Immobilized gp120 activated complement in the absence of lymphocytes.

    Conclusions:

    • Cell-bound HIV-1 gp120 can activate the complement system via the classical pathway in the absence of specific antibodies.
    • Complement activation and subsequent opsonization of gp120-coated CD4+ T cells may contribute to the elimination of non-infected CD4+ T cells in HIV-infected individuals.