T cell exosomes induce cholesterol accumulation in human monocytes via phosphatidylserine receptor

Liudmila Zakharova, Maria Svetlova, Alla F Fomina

Research output: Contribution to journalArticle

90 Citations (Scopus)

Abstract

Activated T lymphocytes release vesicles, termed exosomes, enriched in cholesterol and exposing phosphatidylserine (PS) at their outer membrane leaflet. Although CD4+ activated T lymphocytes infiltrate an atherosclerotic plaque, the effects of T cell exosomes on the atheroma-associated cells are not known. We report here that exosomes isolated from the supernatants of activated human CD4+ T cells enhance cholesterol accumulation in cultured human monocytes and THP-1 cells. Lipid droplets found in the cytosol of exosome-treated monocytes contained both cholesterol ester and free cholesterol. Anti-phosphatidylserine receptor antibodies recognized surface protein on the monocyte plasma membrane and prevented exosome-induced cholesterol accumulation, indicating that exosome internalization is mediated via endogenous phosphatidylserine receptor. The production of proinflammatory cytokine TNF-α enhanced in parallel with monocyte cholesterol accumulation. Our data strongly indicate that exosomes released by activated T cells may represent a powerful, previously unknown, atherogenic factor.

Original languageEnglish (US)
Pages (from-to)174-181
Number of pages8
JournalJournal of Cellular Physiology
Volume212
Issue number1
DOIs
StatePublished - Jul 2007

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Exosomes
T-cells
Monocytes
Cholesterol
T-Lymphocytes
Atherosclerotic Plaques
Cholesterol Esters
Phosphatidylserines
Cell membranes
Membrane Proteins
phosphatidylserine receptor
Cytokines
Cytosol
Membranes
Lipids
Antibodies
Cell Membrane

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology

Cite this

T cell exosomes induce cholesterol accumulation in human monocytes via phosphatidylserine receptor. / Zakharova, Liudmila; Svetlova, Maria; Fomina, Alla F.

In: Journal of Cellular Physiology, Vol. 212, No. 1, 07.2007, p. 174-181.

Research output: Contribution to journalArticle

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