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Characterization of Human Monocyte-derived Dendritic Cells by Imaging Flow Cytometry: A Comparison between Two Monocyte Isolation Protocols
Published on: October 18, 2016
Immune complexes inhibit differentiation, maturation, and function of human monocyte-derived dendritic cells
Evangelina A Laborde1, Silvia Vanzulli, Macarena Beigier-Bompadre
1Laboratory of Immunology, Institute of Hematologic Research, Academia Nacional de Medicina, Buenos Aires, Argentina.
Journal of Immunology (Baltimore, Md. : 1950)
|June 21, 2007
Summary
Immune complexes (IC) alter dendritic cell (DC) development by interacting with Fc receptors. This impairs T cell response and promotes inflammation, potentially contributing to autoimmune diseases.
Area of Science:
- Immunology
- Cell Biology
- Dendritic Cell Biology
Background:
- Immune complexes (IC) binding to Fc gamma receptors (FcgammaRs) on immune cells initiate critical regulatory and effector responses.
- Dendritic cells (DCs) are key antigen-presenting cells that bridge innate and adaptive immunity.
- Dysfunctional DCs are implicated in the pathogenesis of autoimmune disorders.
Purpose of the Study:
- To investigate the impact of IC on the differentiation, maturation, and function of human monocyte-derived DCs.
- To elucidate the specific Fcgamma receptors involved in mediating IC effects on DCs.
- To understand how IC-induced alterations in DCs may contribute to autoimmune disease development.
Main Methods:
- Human monocytes were differentiated into DCs with or without IC.
- Flow cytometry was used to analyze DC surface marker expression (CD1a, CD14, MHC II, CD68, CD83, CD86, CD40).
- Cytokine production (IL-12, IL-10, CCL22, CXCL8, CCL2) and T cell proliferation assays were performed.
Main Results:
- DCs cultured with IC (IC-DC) exhibited altered differentiation, with lower CD1a and higher CD14 and CD68 expression.
- IC binding primarily involved FcgammaRI and FcgammaRII, leading to immature DC phenotypes with high CD83, CD86, and CD40.
- IC-DC showed reduced IL-12 production, impaired endocytic activity, and decreased T cell proliferation, alongside a proinflammatory cytokine profile.
Conclusions:
- IC significantly disrupt DC differentiation and maturation, skewing them towards a proinflammatory phenotype.
- This IC-induced DC dysfunction, characterized by impaired antigen presentation and T cell activation, mirrors DC states in autoimmune diseases like lupus and arthritis.
- Altered DC maturation by IC may play a crucial role in the pathogenesis of autoimmune diseases.
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