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Related Experiment Video

Updated: May 7, 2026

Generation of Human Monocyte-derived Dendritic Cells from Whole Blood

Generation of Human Monocyte-derived Dendritic Cells from Whole Blood

Published on: December 24, 2016

HIV impairs CD34+-derived monocytic precursor differentiation into functional dendritic cells.

V Bordoni¹, G Castelli, E Montesoro

¹Cellular Immunology Laboratory, National Institute for Infectious Diseases L.Spallanzani, IRCCS, Rome, Italy.

International Journal of Immunopathology and Pharmacology

|September 27, 2013

Summary

Human immunodeficiency virus (HIV) infection impairs the development of functional dendritic cells (DCs) from hematopoietic progenitor cells. HIV-infected precursors generate DCs with reduced proliferation and impaired T-cell stimulation, contributing to immune suppression.

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Isolation, Transfection, and Culture of Primary Human Monocytes

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Isolation, Transfection, and Culture of Primary Human Monocytes

Isolation, Transfection, and Culture of Primary Human Monocytes

Published on: December 16, 2019

Area of Science:

Immunology
Virology
Cell Biology

Background:

Dendritic cells (DCs) are crucial for initiating T-cell-dependent immune responses.
Previous studies suggest human immunodeficiency virus (HIV) impairs DC maturation and function.
Monocytic (Mo) differentiating cells are known to efficiently replicate monocytotropic HIV strains.

Purpose of the Study:

To investigate the impact of HIV infection on dendritic cell (DC) function during development from hematopoietic progenitors.
To determine if HIV-infected monocytic precursors (MoP) can generate functional DCs.

Main Methods:

Developed an in vitro culture system using CD34+ hematopoietic progenitor cells (HPCs).
Induced monocytic differentiation and infected early-stage monocytic precursors (MoP) with an M-tropic HIV strain (BaL).
Switched infected MoP to DC differentiation using GM-CSF and IL-4, then assessed DC viability, proliferation, HIV-p24 production, and T-cell stimulation.

Main Results:

Derived DCs were actively infected, confirmed by HIV-p24 production.
HIV infection did not significantly affect cell viability but reduced cell proliferation.
HIV-infected MoP generated DCs with inefficient functional activity, including reduced uptake capability and impaired allogeneic T-cell stimulation.

Conclusions:

HIV-infected monocytic precursors (MoP) lose the capacity to generate functional dendritic cells (DCs).
This impaired DC development represents a significant mechanism of HIV-induced immunosuppression.
Understanding this process is critical for developing therapeutic strategies against HIV.