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Antigen presenting cell function in HIV-1 infected patients.

S J Fidler1, A D Rees

  • 1Department Genito-Urinary Medicine and Communicable Diseases, Imperial College, School of Medicine at St Mary's Hospital, London, UK.

Immunology Letters
|April 15, 1999
PubMed
Summary

Antigen presenting cells (APCs) in HIV-1 patients show defects in presenting peptides to CD4 T-cells. This impairment, linked to gp120 binding, worsens with viral load and impacts anti-viral immunity.

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Area of Science:

  • Immunology
  • Virology
  • Cellular Biology

Background:

  • Antigen presenting cell (APC) function is critical for initiating adaptive immune responses, including cytotoxic T-cell activation and antibody production.
  • Previous research has indicated potential dysfunctions in APCs from individuals with Human Immunodeficiency Virus type 1 (HIV-1) infection.

Purpose of the Study:

  • To investigate the functional capacity of APCs from HIV-1 infected patients in presenting peptides to CD4 T-cell clones.
  • To elucidate the mechanism underlying APC defects in HIV-1 infection and their correlation with disease progression.

Main Methods:

  • Evaluation of APC function by assessing peptide presentation to a panel of well-defined CD4 T-cell clones.
  • Analysis of T-cell clone susceptibility to APC defects and correlation with anti-CD4 antibody inhibition.

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  • Investigation of the role of APC-associated gp120 in T-cell CD4 binding.

    • Main Results:

    • APCs from HIV-1 infected patients demonstrated a reduced capacity to present peptides to CD4 T-cell clones.
    • This APC defect was observed early in infection and exacerbated with increased viral load, correlating with disease progression.
    • Differential susceptibility of CD4 T-cell clones to the APC defect was noted, with some clones being significantly more sensitive to inhibition.

    Conclusions:

    • The findings suggest that APC dysfunction is an early and progressive feature of HIV-1 infection, potentially influencing anti-viral efficacy.
    • The data strongly support a mechanism where binding of T-cell CD4 by APC-associated gp120 underlies the observed APC defect.
    • Understanding this mechanism is crucial for developing therapeutic strategies to restore immune function in HIV-1 patients.