PPARγ modulated inflammatory response of human dendritic cell subsets to engulfed apoptotic neutrophils

Gyöngyike Majai, Péter Gogolák, Csilla Ambrus, György Vereb, Judit Hodrea, László Fésüs, Éva Rajnavölgyi

Research output: Contribution to journalArticle

19 Citations (Scopus)


The means of how phagocytes handle apoptotic cells has a great impact on the outcome of immune responses. Here, we show that phagocytosis of allogeneic, apoptotic neutrophils by human monocyte-derived DCs is slow and less efficient than that of macrophages, and CD1a- DCs are more active in the engulfment of apoptotic neutrophils than CD1a+ DCs. Blocking DC-SIGN function partially interferes with the uptake of apoptotic cells, and long-term interaction of apoptotic neutrophils with DCs makes them prone to proinflammatory cytokine responses. Engulfment of apoptotic cells sensitizes CD1a- DCs for high IL-8, TNF-α, IL-6, and CD1a+ cells for IL-12 and IL-10 cytokine secretion elicited by additional inflammatory stimuli, which also result in the polarization of autologous T lymphocytes to Th1 effector cells. Ligand-induced activation of PPARγ by RSG results in enhanced phagocytosis, but the proinflammatory response and the capacity to trigger Th1 cell activation of CD1a- DCs are not enhanced. These results demonstrate that DCs are able to respond to allogeneic, apoptotic neutrophils with inflammatory cytokines and T cell responses in a subtype-specific manner that is modulated by the anti-inflammatory effects of PPARγ.

Original languageEnglish
Pages (from-to)981-991
Number of pages11
JournalJournal of Leukocyte Biology
Issue number5
Publication statusPublished - Nov 1 2010


  • Inflammation
  • Phagocytosis
  • T lymphocyte

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Cell Biology

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