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Monocytes complexed to platelets differentiate into functionally deficient dendritic cells.

Meera V Singh1, Sumanun Suwunnakorn1,2, Sydney R Simpson1

  • 1Department of Microbiology and Immunology, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA.

Journal of Leukocyte Biology
|July 15, 2020
PubMed
Summary
This summary is machine-generated.

Activated platelets impair the development of functional dendritic cells (DCs) from monocytes, hindering effective T cell responses and potentially impacting HIV immunity. Strategies to disrupt platelet-monocyte complexes may improve DC function for enhanced immunization.

Keywords:
CD40LHIV infectionimmunotherapyplatelet-monocyte complexes

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Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Platelets release immunoregulatory molecules upon activation.
  • Activated platelets form complexes with monocytes, inducing a proinflammatory phenotype, particularly in HIV-infected individuals.
  • Monocytes are crucial precursors for dendritic cells (DCs), essential for immune responses and vaccine development.

Purpose of the Study:

  • To investigate the impact of activated platelets on monocyte differentiation into functional DCs.
  • To assess the immunoregulatory effects of platelet-monocyte complexes (PMCs) on DC development and function.

Main Methods:

  • In vitro culture of DCs from monocytes, some complexed with activated platelets.
  • Analysis of DC surface marker expression (e.g., CD206, CD80, CD86, CCR7).
  • Assessment of antigen uptake, T cell activation capacity, and cytokine secretion (IL-12p70).

Main Results:

  • DCs derived from PMCs showed reduced expression of critical DC function molecules.
  • Reduced antigen uptake capacity was observed in PMC-derived DCs.
  • Impaired ability of PMC-derived DCs to activate T cells and promote type-1 immune responses to HIV antigens.

Conclusions:

  • Formation of PMCs suppresses the development of functional DCs from monocytes.
  • Disruption of PMCs, through antiplatelet drugs or using platelet-free monocytes, could enhance DC function.
  • This approach may improve immunization strategies and augment immune control of HIV.