Mediators involved in the immunomodulatory effects of apoptotic cells. - Archive ouverte HAL Access content directly
Journal Articles Transplantation Year : 2007

Mediators involved in the immunomodulatory effects of apoptotic cells.

(1) , (1) , (1) , (1) , (1, 2)
1
2

Abstract

Immunomodulatory properties are attributed to apoptotic cells. These properties have been used to modulate allogeneic immune responses in experimental transplantation settings. In independent studies, apoptotic cell infusion has been shown to favor hematopoietic cell engraftment, to increase heart graft survival, and to delay the lethal onset of graft-versus-host disease (GVHD). The goal of this review was to discuss how apoptotic cell infusion interferes with graft rejection or host rejection (i.e., GVHD) and to focus on the potential mediators or "perpetuators" involved in apoptotic cell-induced immunomodulation. Particular emphasis on apoptotic cell phagocytosis, transforming growth factor (TGF)-beta secretion, and regulatory T cell induction was performed. Stimulating "naturally" immunosuppressive molecules (i.e., TGF-beta) or immunomodulatory cells ("alternatively-activated" macrophages, certain dendritic cell subsets, or regulatory T cells) in a physiological manner by using apoptotic cell infusion can be a promising way to induce tolerance.
Fichier principal
Vignette du fichier
P_Saas_Transplantation_2007.pdf (308 Ko) Télécharger le fichier
Vignette du fichier
inserm-00479706_edited.pdf (278.85 Ko) Télécharger le fichier
Origin : Files produced by the author(s)
Origin : Files produced by the author(s)
Loading...

Dates and versions

inserm-00479706 , version 1 (20-02-2012)

Identifiers

Cite

Philippe Saas, Francis Bonnefoy, Stephanie Kury-Paulin, François M. Kleinclauss, Sylvain Perruche. Mediators involved in the immunomodulatory effects of apoptotic cells.. Transplantation, 2007, 84 (1 Suppl), pp.S31-4. ⟨10.1097/01.tp.0000269113.59857.d6⟩. ⟨inserm-00479706⟩

Collections

INSERM UNIV-FCOMTE
127 View
643 Download

Altmetric

Share

Gmail Facebook Twitter LinkedIn More