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1.

001-es BibID:BIBFORM028776
Első szerző:Ludányi Katalin (immunológus)
Cím:Ligation of RARgamma inhibits proliferation of phytohaemagglutinin-stimulated T-cells via down-regulating JAK3 protein levels / Katalin Ludányi, Zsuzsanna S. Nagy, Magdolna Alexa, Uwe Reichert, Serge Michel, László Fésüs, Zsuzsa Szondy
Dátum:2005
ISSN:0165-2478
Megjegyzések:The mechanisms whereby Vitamin A regulates the immune system are poorly understood. We have shown previously that retinoic acids, the Vitamin A derivatives, promote both apoptosis of neglected thymocytes and the activation-induced cell death of peripheral T-cells via ligating the nuclear retinoid receptor (RAR) gamma. In the present study, we found that human peripheral T-cells express RARalpha and gamma, but not RARbeta. Increasing concentrations of 9-cis RA inhibited phytohaemagglutinin (PHA)-induced proliferation of T-cells, an effect that could be mimicked only by addition of RARgamma agonists and could be inhibited by an RARgamma antagonist. Interleukin-2 (IL-2) produced is known to mediate PHA-induced proliferation of T lymphocytes. Ligation of RARgamma did not affect the PHA-induced high affinity IL-2 receptor expression, slightly reduced the PHA-induced IL-2 production, but interfered with the IL-2-mediated signal transduction resulting in inhibition of PHA-induced phosphorylation of retinoblastoma protein and of up-regulation of Bcl-2. Janus kinases JAK1 and JAK3 play a determinant role in IL-2-dependent signal transduction. Ligation of RARgamma did not affect the levels of JAK1, but prevented IL-2-induced expression of JAK3 resulting in inhibition of PHA-induced phosphorylation of Stat5 molecules. Our data suggest that the previously observed toxic effect of high concentrations of retinoids on the immune system might be mediated via formation of 9-cis RA, which via ligation of RARgamma not only induces cell death in immature thymocytes, but inhibits proliferation of T-cells as well.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Immunology Letters. - 98 : 1 (2005), p. 103-113. -
További szerzők:Nagy Zsuzsanna (1973-) (okleveles középiskolai kémia-fizika szakos tanár) Alexa Magdolna Reichert, Uwe Michel, Serge Fésüs László (1947-) (orvos biokémikus) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus)
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2.

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)
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3.

001-es BibID:BIBFORM060601
Első szerző:Szegezdi Éva
Cím:Ligation of Retinoic Acid Receptor [alfa] Regulates Negative Selection of Thymocytes by Inhibiting Both DNA Binding of nur77 and Synthesis of Bim / Éva Szegezdi, Ildikó Kiss, Ágnes Simon, Bernadett Blaskó, Uwe Reichert, Serge Michel, Mátyás Sándor, László Fésüs, Zsuzsa Szondy
Dátum:2003
ISSN:0022-1767 1550-6606
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Immunology. - 170 : 7 (2003), p. 3577-3584. -
További szerzők:Kiss Ildikó (biokémikus) Simon Ágnes (1969-) (laboratóriumi szakorvos) Blaskó Bernadett Reichert, Uwe Michel, Serge Sándor Mátyás Fésüs László (1947-) (orvos biokémikus) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus)
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4.

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)
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5.

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)
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6.

001-es BibID:BIBFORM028765
Első szerző:Szondy Zsuzsanna (molekuláris sejtbiológus, biokémikus)
Cím:Retinoic acids regulate apoptosis of T lymphocytes through an interplay between RAR and RXR receptors / Zsuzsa Szondy, Uwe Reichert, László Fésüs
Dátum:1998
ISSN:1350-9047
Megjegyzések:Vitamin A deficiency has been known for a long time to be accompanied with immune deficiency and susceptibility to a wide range of infectious diseases. Increasing evidence suggests that retinoic acids derived from vitamin A are involved in the functional regulation of the immune system. Of the two groups of retinoid receptors, retinoic acid receptors (RARs) and retinoid X receptors (RXRs) all-trans and 9-cis retinoic acids are high affinity ligands for RARs and 9-cis retinoic acid additionally binds to RXRs. In cells, at high concentrations, all-trans retinoic acid can be converted to 9-cis retinoic acid by unknown mechanisms. Apoptosis plays a major role in shaping the T cell repertoire and one way in which retinoids may affect immune functions is to influence the various apoptosis pathways. Indeed, it has been shown that retinoic acids can induce apoptosis, increase the rate of dexamethasone-induced death and inhibit activation-induced death of thymocytes and T lymphocytes. Therefore, retinoids together with glucocorticoids may be involved in regulating positive and negative selection of T lymphocytes. Here we demonstrate that retinoids can induce apoptosis of T cells through the stimulation of RARgamma. Specific stimulation of RARalpha, on the other hand, prevents both RARgamma-dependent and TCR-mediated cell death. In all these functions 9-cis retinoic acid proved to be more effective than all-trans retinoic acid suggesting the involvement of RXRs. Based on these results a possible mechanism through which costimulation of RARs and RXRs might affect spontaneous and activation-induced death of T lymphocytes is proposed.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Cell Death And Differentiation. - 5 : 1 (1998), p. 4-10. -
További szerzők:Reichert, Uwe Fésüs László (1947-) (orvos biokémikus)
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7.

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)
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8.

001-es BibID:BIBFORM028775
Első szerző:Tóth Beáta
Cím:Retinoids induce Fas(CD95) ligand cell surface expression via RARgamma and nur77 in T cells / Beáta Tóth, Katalin Ludányi, Ildikó Kiss, Uwe Reichert, Serge Michel, László Fésüs, Zsuzsa Szondy
Dátum:2004
ISSN:0014-2980
Megjegyzések:Cells from the CD4+ murine T hybridoma line IP-12-7 enter the apoptotic suicide program via the Fas ligand (FasL)/Fas-mediated pathway upon TCR stimulation. This stimulus regulates the sensitization of the Fas death pathway and the cell surface appearance of preformed FasL. The apoptosis is dependent on new mRNA and protein synthesis and involves up-regulation of nur77. Two groups of nuclear receptors for retinoic acids (RA) have been identified: retinoic acid receptors (RAR) and retinoid X receptors. IP-12-7 cells express RARalpha and RARgamma. Here we show that,in the IP-12-7 T cells, RA also induced the expression and DNA binding of nur77, and the cell surface appearance of FasL. The induction was mediated via RARgamma. Despite the induced expression of cell surface FasL, only two structurally related RARgamma-selective compounds, CD437 and CD2325, initiated apoptosis in these cells. The lack of apoptosis induction by natural RA was related to the inability of RARgamma to sensitize the Fas death-pathway. Cell surface FasL, however, was able to induce cell death in Fas-bearing target cells. Natural RA also induced the expression of FasL in phytohemagglutinin-activated peripheral murine T cells. It is proposed that therapeutically administered RA might induce apoptosis in Fas-sensitive cells via induction of FasL expression in activated Tcells.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:European Journal of Immunology. - 34 : 3 (2004), p. 827-836. -
További szerzők:Ludányi Katalin (1975-) (immunológus) Kiss Ildikó (biokémikus) Reichert, Uwe Michel, Serge Fésüs László (1947-) (orvos biokémikus) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus)
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