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001-es BibID:BIBFORM020979
Első szerző:Hodrea Judit (vegyész)
Cím:The glucocorticoid dexamethasone programs human dendritic cells for enhanced phagocytosis of apoptotic neutrophils and inflammatory response / Judit Hodrea, Gyöngyike Majai, Zoltán Doró, Gábor Zahuczky, Attila Pap, Éva Rajnavölgyi, László Fésüs
Dátum:2012
ISSN:0741-5400
Megjegyzések:Glucocorticoids are powerful anti-inflammatory compounds inhibiting inflammatory cell recruitment and production of pro-inflammatory cytokines. We have recently found that dendritic cells, the key-players of T cell priming and polarization respond to allogeneic apoptotic neutrophils with proinflammatory cytokine release and Th1 cell activation. Here we show that monocyte-derived human dendritic cells develop their capacity to engulf apoptotic cells by up-regulating a set of apopto-phagocytic genes. This gene expression pattern was reprogrammed when differentiation took place in the presence of the synthetic glucocorticoid dexamethasone (Dex) which increased the expression of phagocytosis receptors MERTK and CD14, the bridging molecule C1QA, DNASE2 and the adenosine A3 receptor (ADORA3). The increased phagocytosis was attenuated by the addition of ADORA3 antagonist and could not be observed when bone marrow derived dendritic cells of ADORA3 knockout mice were treated with Dex. The glucocorticoid treated human dendritic cells loaded with allogeneic apoptotic neutrophils secreted, in response to LPS and IFN, the inflammatory cytokine TNFα. Furthermore, the Dex treated dendritic cells could activate autologous T lymphocytes toward Th1 effector cells and this was enhanced by their exposure to allogeneic apoptotic neutrophils.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekuláris Medicina
Megjelenés:Journal Of Leukocyte Biology. - 91 : 1 (2012), p. 127-136. -
További szerzők:Majai Gyöngyike (1977-) (belgyógyász, immunológus) Doró Zoltán (1981-) (biotechnológus) Zahuczky Gábor (1975-) (molekuláris biológus, biokémikus, vegyész) Pap Attila (1980-) (biológus) Rajnavölgyi Éva (1950-) (immunológus) Fésüs László (1947-) (orvos biokémikus)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Jelátviteli kapcsolatok ős- és dendritikus sejt altípusokban
Collaboration of signalling pathways in stem- and dendritic cell subsets
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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2.

001-es BibID:BIBFORM051720
035-os BibID:PMID:23775590
Első szerző:Kristóf Endre (általános orvos)
Cím:Novel role of ICAM3 and LFA-1 in the clearance of apoptotic neutrophils by human macrophages / Endre Kristóf, Gábor Zahuczky, Klára Katona, Zoltán Doró, Éva Nagy, László Fésüs
Dátum:2013
ISSN:1360-8185
Megjegyzések:Apoptotic cells express eat-me signals which are recognized by several receptors mainly on professional phagocytes of the mononuclear phagocyte system. This "engulfment synapse" can define a safe and effective clearance of apoptotic cells in order to maintain tissue homeostasis in the entire body. We show that the expression of four genes related to apoptotic cell clearance is strongly up-regulated in human macrophages 30 min after administration of apoptotic neutrophils. Out of these the significant role of the up-regulated intercellular adhesion molecule 3 (ICAM3) in phagocytosis of apoptotic neutrophils could be demonstrated in macrophages by gene silencing as well as treatment with blocking antibodies. Blocking ICAM3 on the surface of apoptotic neutrophils also resulted in their decreased uptake which confirmed its role as an eat-me signal expressed by apoptotic cells. In macrophages but not in neutrophils silencing and blocking integrin alphaL and beta2 components of lymphocyte function-associated antigen 1 (LFA-1), which can strongly bind ICAM3, resulted in a decreased phagocytosis of apoptotic cells indicating its possible role to recognize ICAM3 on the surface of apoptotic neutrophils. Finally, we report that engulfing portals formed in macrophages during phagocytosis are characterized by accumulation of ICAM3, integrin alphaL and beta2 which show co-localization on the surface of phagocytes. Furthermore, their simultaneous knock-down in macrophages resulted in a marked deficiency in phagocytosis and a slight decrease in the anti-inflammatory effect of apoptotic neutrophils. We propose that ICAM3 and LFA-1 act as recognition receptors in the phagocytosis portals of macrophages for engulfment of apoptotic neutrophils.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekuláris Medicina
Doktori iskola
Megjelenés:Apoptosis. - 18 : 10 (2013), p. 1235-1251. -
További szerzők:Zahuczky Gábor (1975-) (molekuláris biológus, biokémikus, vegyész) Katona Klára (1976-) Doró Zoltán (1981-) (biotechnológus) Nagy Éva (1980-) (molekuláris biológus) Fésüs László (1947-) (orvos biokémikus)
Pályázati támogatás:NK 105046
OTKA
K 61868
OTKA
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Az apoptózis molekuláris mechanizmusa
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
Molekuláris Sejt- és Immunbiológiai Doktori Iskola
TRANSCOM IAPP251506
FP7
TRANSPATH ITN 289964
FP7
NKTH NTP Schizo08
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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