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Effect of HIV on antigen presentation by dendritic cells and macrophages
1Antigen Presentation Research Group, Clinical Research Centre, Harrow, UK.
Insights
Dendritic cells (DCs) infected with HIV lose their ability to stimulate immune responses, while macrophages (MOs) retain this function. This suggests MOs may present antigens early in HIV infection, but impaired DCs could lead to cumulative T-cell loss.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Dendritic cells (DCs) and macrophages (MOs) are crucial antigen-presenting cells.
- Human Immunodeficiency Virus (HIV) targets immune cells, impacting immune function.
- Understanding antigen presentation during HIV infection is vital for therapeutic strategies.
Purpose of the Study:
- To investigate the antigen-presenting capacity of dendritic cells (DCs) and macrophages (MOs) after in vitro HIV infection.
- To compare the functional impairment of DCs and MOs in response to HIV.
Main Methods:
- In vitro infection of DCs and MOs with HIV.
- Assessment of cellular infection using in situ hybridization.
- Evaluation of antigen-presenting function via mixed leukocyte reactions and recall antigen stimulation assays.
Main Results:
- DCs, but not MOs, stimulated primary allogeneic lymphocyte responses in non-infected cells.
- Both DCs and MOs presented recall antigens (influenza, tetanus toxoid) to autologous T lymphocytes.
- HIV infection impaired DC antigen presentation to alloantigens and recall antigens.
- HIV-infected MOs retained their ability to present recall antigens.
Conclusions:
- HIV-infected DCs lose their antigen-presenting function, potentially hindering adaptive immune responses.
- Macrophages maintain antigen-presenting capabilities post-HIV infection, possibly supporting early immune responses.
- Impaired DC function during HIV infection may lead to cumulative T-cell damage due to a compromised ability to recruit resting T cells.
Abstract:
The antigen-presenting function of dendritic cells (DC) and macrophages (MO) following infection with HIV in vitro was examined. Using non-infected cells, DC, but not MO, stimulated primary proliferative responses in allogeneic lymphocytes in the mixed leukocyte reaction. Both DC and MO stimulated secondary responses to influenza virus and to tetanus toxoid in autologous T lymphocytes. After exposure of DC and MO to HIV1 in vitro for 2 days, 27% of DC but less than 1% MO became infected as assessed by in situ hybridization. DC were blocked in their capacity to stimulate responses to alloantigens or to the recall antigens. By contrast, MO retained the ability to stimulate responses to the recall antigens. Similar effects during in vivo infection would allow activated T-cell clones to respond to antigens presented by MO early in infection. However, any loss of activated T cells might prove cumulative and damaging in the absence of an effective DC recruitment mechanism for resting T cells.
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