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1.

001-es BibID:BIBFORM028771
Első szerző:Révészné Tóth Réka (molekuláris biológus, biokémikus)
Cím:Activation-induced apoptosis and cell surface expression of Fas (CD95) ligand are reciprocally regulated by retinoic acid receptor alpha and gamma and involve nur77 in T cells / Réka Tóth, Éva Szegezdi, Uwe Reichert, Jean-Michel Bernardon, Serge Michel, Philippe Ancian, Katalin Kis-Tóth, Zsolt Macsári, László Fésüs, Zsuzsa Szondy
Dátum:2001
ISSN:0014-2980
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:European Journal of Immunology. - 31 : 5 (2001), p. 1382-1391. -
További szerzők:Szegezdi Éva Reichert, Uwe Bernardon, Jean Michel Michel, Serge Ancian, Philippe Kis-Tóth Katalin (1975-) (immunológus) Macsári Zsolt Fésüs László (1947-) (orvos biokémikus) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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2.

001-es BibID:BIBFORM028783
Első szerző:Szondy Zsuzsanna (molekuláris sejtbiológus, biokémikus)
Cím:Cell death in HIV pathogenesis and its modulation by retinoids / Zsuzsa Szondy, Réka Tóth, Éva Szegezdi, Uwe Reichert, Philippe Ancian, László Fésüs
Dátum:2001
Megjegyzések:Patients infected with the human immunodeficiency virus exhibit a progressive decline in the CD4 T-cell number, resulting in immunodeficiency and increased susceptibility to opportunistic infections and malignancies. Although CD4 T cell production is impaired in patients infected with HIV, there is now increasing evidence that the primary basis of T cell depletion is accelerated apoptosis of CD4 and CD8 T cells. The rate of lymphocyte apoptosis in HIV infection correlates inversely with the progression of the disease: it is low in long-term progressors and in patients undergoing highly active antiretroviral therapy. Interestingly, only a minor fraction of apoptotic lymphocytes are infected by HIV, indicating that the enhanced apoptosis does not necessarily always serve to remove the HIV+ cells and results from mechanisms other than direct infection. Thus, understanding and influencing the mechanisms of HIV-associated lymphocyte apoptosis may lead to new therapies for HIV disease. In this paper the potential effects of retinoids on CD4 T cell apoptosis is discussed.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
apoptosis
CD4 T cells
CD95 ligand
retinoic acid
nur77
HIV
Megjelenés:Annals of the New York Academy of Sciences. - 946 (2001), p. 95-107. -
További szerzők:Révészné Tóth Réka (1969-) (molekuláris biológus, biokémikus) Szegezdi Éva Reichert, Uwe Ancian, Philippe Fésüs László (1947-) (orvos biokémikus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM028766
Első szerző:Szondy Zsuzsanna (molekuláris sejtbiológus, biokémikus)
Cím:Inhibition of activation-induced apoptosis of thymocytes by all-trans- and 9-cis-retinoic acid is mediated via retinoic acid receptor alpha / Zsuzsa Szondy, Uwe Reichert, Jean-Michel Bernardon, Serge Michel, Réka Tóth, Éva Karászi, László Fésüs
Dátum:1998
ISSN:0264-6021
Megjegyzések:Thymocytes can be induced to undergo apoptotic cell death by activation through the T-cell receptor (TCR). This process requires macromolecular synthesis and has been shown to be inhibited by retinoic acids (RAs). Two groups of nuclear receptors for RAs have been identified: retinoic acid receptors (RARs) and retinoid X receptors (RXRs). All-trans-RA is the high-affinity ligand for RARs, and 9-cis-RA additionally binds to RXRs with high affinity. Because 9-cis-RA is much more potent in inhibiting TCR-mediated death than all-trans-RA, it was suggested that RXRs participate in the process. In the present study various synthetic retinoid analogues were used to address this question further. The results presented suggest that the inhibitory effect of RAs on activation-induced death of thymocytes is mediated via RARalpha, because (1) it can be reproduced by various RARalpha analogues both in vitro and in vivo, (2) the effect of RAs can be inhibited by the addition of an RARalpha antagonist, (3) CD4+CD8+thymocytes, which die on TCR stimulation, express RARalpha. Stimulation of RARgamma, in contrast, enhances the activation-induced death of thymocytes and inhibits its prevention by RARalpha stimulation. RXR co-stimulation suspends this inhibitory effect of RARgamma and permits the preventive function of RARalpha on activation-induced death. Our results suggest a complex interaction between the various isoforms of retinoid receptors and demonstrate that low (physiological) concentrations of all-trans-RA do not affect the activation-induced death of thymocytes because the RARalpha-mediated inhibitory and the RARgamma-mediated enhancing pathways are in balance, whereas if 9-cis-RA is formed, additional stimulation of RXRs permits the inhibitory action of RARalpha.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Biochemical Journal. - 331 : 3 (1998), p. 767-774. -
További szerzők:Reichert, Uwe Bernardon, Jean Michel Michel, Serge Révészné Tóth Réka (1969-) (molekuláris biológus, biokémikus) Karászi Éva Fésüs László (1947-) (orvos biokémikus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM028733
Első szerző:Szondy Zsuzsanna (molekuláris sejtbiológus, biokémikus)
Cím:Induction of apoptosis by retinoids and retinoic acid receptor gamma-selective compounds in mouse thymocytes through a novel apoptosis pathway / Zsuzsa Szondy, Uwe Reichert, Jean-Michel Bernardon, Serge Michel, Réka Tóth, Philippe Ancian, Eva Ajzner, Laszlo Fesus
Dátum:1997
ISSN:0026-895X
Megjegyzések:Retinoic acids are morphogenic signaling molecules that are derived from vitamin A and involved in a variety of tissue functions. Two groups of their nuclear receptors have been identified: retinoic acid receptors (RARs) and retinoic acid X receptors (RXRs). All-trans retinoic acid is the high affinity ligand for RARs, and 9-cis retinoic acid also binds to RXRs with high affinity. In cells at high concentrations, all-trans retinoic acid can be converted to 9-cis retinoic acid via unknown mechanisms. It was previously shown that retinoic acids prevents activation-induced death of thymocytes. Here, we report that both all-trans and 9-cis retinoic acid induce apoptosis of mouse thymocytes and purified CD4+CD8+ cells in ex vivo cultures, with 9-cis retinoic acid being 50 times more effective. The induction of apoptosis by retinoic acids is mediated by RARgamma because (a) the phenomenon can be reproduced only by RARgamma-selective retinoic acid analogs, (b) the cell death induced by either retinoic acids or RARgamma analogs can be inhibited by RARgamma-specific antagonists, and (c) CD4+CD8+ thymocytes express RARgamma. In vivo administration of an RARgamma analog resulted in thymus involution with the concomitant activation of the apoptosis-related endonuclease and induction of tissue transglutaminase. The RARgamma pathway of apoptosis is RNA and protein synthesis dependent, affects the CD4+CD8+ double positive thymocytes, and can be inhibited by the addition of either Ca2+ chelators or protease inhibitors. Using various RAR- and RXR-specific analogs and antagonists, it was demonstrated that stimulation of RAR alpha inhibits the RARgamma-specific death pathway (which explains the lack of apoptosis stimulatory effects of all-trans retinoic acid at physiological concentrations) and that costimulation of the RXR receptors (in the case of 9-cis retinoic acid) can neutralize this inhibitory effect. It is suggested that formation of 9-cis retinoic acid may be a critical element in regulating both the positive selection and the "default cell death pathway" of thymocytes.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Molecular Pharmacology. - 51 : 6 (1997), p. 972-982. -
További szerzők:Reichert, Uwe Bernardon, Jean Michel Michel, Serge Révészné Tóth Réka (1969-) (molekuláris biológus, biokémikus) Ancian, Philippe Ajzner Éva (1968-) (laboratóriumi szakorvos) Fésüs László (1947-) (orvos biokémikus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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