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Related Experiment Videos

Follicular dendritic cell function and murine AIDS

A Masuda1, G F Burton, B A Fuchs

  • 1Department of Microbiology and Immunology, Medical College of Virginia/Virginia Commonwealth University, Richmond 23298.

Immunology
|January 1, 1994
PubMed
Summary
This summary is machine-generated.

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Murine acquired immune deficiency syndrome (MAIDS) impairs follicular dendritic cell (FDC) functions, including antigen retention and antibody maintenance. However, FDCs from infected mice retain co-stimulatory capacity, potentially driving MAIDS pathology.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Murine acquired immune deficiency syndrome (MAIDS) is an LP-BM5 retrovirus-induced immunodeficiency in mice.
  • Follicular dendritic cells (FDCs) play a crucial role in adaptive immunity by trapping and presenting antigens.
  • The impact of MAIDS on FDC function remains incompletely understood.

Purpose of the Study:

  • To investigate the functional alterations of FDCs during MAIDS.
  • To determine if retroviral infection affects FDC's antigen trapping, retention, and co-stimulatory capabilities.
  • To elucidate the potential role of FDC dysfunction in MAIDS pathogenesis.

Main Methods:

  • Mice were infected with LP-BM5 retrovirus to induce MAIDS.
  • FDC antigen trapping and retention were assessed using radiolabeled antigen (HSA).

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  • Serum antibody levels and B-cell proliferation in response to FDC co-stimulation were measured.

    • Main Results:

    • FDCs from MAIDS mice showed significantly reduced ability to trap and retain antigens starting from 3 weeks post-infection.
    • Serum antibody titers specific to trapped antigens declined precipitously after 3 weeks.
    • Despite impaired antigen handling, FDCs from infected mice retained their capacity to provide co-stimulatory signals to B cells.

    Conclusions:

    • LP-BM5 retrovirus infection markedly impairs FDC antigen-presenting functions in MAIDS.
    • The retained co-stimulatory function of FDCs in MAIDS may contribute to characteristic lymphadenopathy and splenomegaly.
    • These findings highlight a critical role for FDC dysfunction in the development of MAIDS.