Integrating systemic information at the molecular level: Cross-talk between steroid receptors and cytokine signaling on different target cells
An essential event in immune activation is the increase of cytokines in both plasma and immune tissues. Steroid hormones influence several adaptive responses in both health and disease. Cytokines and steroids have an intimate cross-communication in many systems, making possible a satisfactory adapti...
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| Otros Autores: | , , , , , , , , |
| Formato: | Capítulo de libro |
| Lenguaje: | Inglés |
| Publicado: |
New York Academy of Sciences
2003
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| Acceso en línea: | Registro en Scopus DOI Handle Registro en la Biblioteca Digital |
| Aporte de: | Registro referencial: Solicitar el recurso aquí |
| LEADER | 10809caa a22012737a 4500 | ||
|---|---|---|---|
| 001 | PAPER-4935 | ||
| 003 | AR-BaUEN | ||
| 005 | 20230518203432.0 | ||
| 008 | 190411s2003 xx ||||fo|||| 00| 0 eng|d | ||
| 024 | 7 | |2 scopus |a 2-s2.0-0038468332 | |
| 024 | 7 | |2 cas |a cyclic AMP, 60-92-4; cyclic AMP dependent protein kinase; cyclic AMP responsive element binding protein, 130428-87-4, 130939-96-7; Smad4 protein, 282562-18-9; transcription factor GATA 3, 137878-55-8 | |
| 040 | |a Scopus |b spa |c AR-BaUEN |d AR-BaUEN | ||
| 030 | |a ANYAA | ||
| 100 | 1 | |a Refojo, D. | |
| 245 | 1 | 0 | |a Integrating systemic information at the molecular level: Cross-talk between steroid receptors and cytokine signaling on different target cells |
| 260 | |b New York Academy of Sciences |c 2003 | ||
| 270 | 1 | 0 | |m Arzt, E.; Lab. Fisiol. y Biol. Molecular, FCEN-Universidad de Buenos Aires, Pabellón II (C1428EHA), Buenos Aires, Argentina; email: earzt@fbmc.fcen.uba.ar |
| 506 | |2 openaire |e Política editorial | ||
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| 504 | |a Costas, M., Trapp, T., Paez Pereda, M., Molecular and functional evidence for in vitro cytokine enhancement of human and murine target cell sensitivity to glucocorticoids: TNF-α priming increases glucocorticoid inhibition of TNF-α-induced cytotoxicity/apoptosis (1996) J. Clin. Invest., 98, pp. 1409-1416 | ||
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| 504 | |a Zacharchuk, C.M., Mercep, M., Chakraborti, P., Programmed T lymphocyte death: Cell activation and steroid-induced pathways are mutually antagonistic (1990) J. Immunol., 145, pp. 4037-4045 | ||
| 504 | |a Ashwell, J.D., Lu, F.W.M., Vacchio, M.S., Glucocorticoids in T-cell development and function (2000) Ann. Rev. Immunol., 18, pp. 309-345 | ||
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| 504 | |a Kasibhatla, S., Genestier, L., Green, D.R., Regulation of fas-ligand expression during activation-induced cell death in T lymphocytes via nuclear factor kappaB (1999) J. Biol. Chem., 274, pp. 987-992 | ||
| 504 | |a Müller-Igaz, L., Refojo, D., Costas, M., CRE-mediated transcriptional activation is involved in cAMP protection of T-cell receptor-induced apoptosis but not in cAMP potentiation of glucocorticoid-mediated programmed cell death (2002) Biochim. Biophys. Acta, 1542, pp. 139-148 | ||
| 504 | |a Glimcher, L.H., Murphy, K.M., Lineage commitment in the immune system: The T helper lymphocyte grows up (2000) Genes Dev., 14, pp. 1693-1711 | ||
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| 504 | |a Zheng, W., Flavell, R.A., The transcription factor GATA-3 is necessary and sufficient for Th2 cytokine gene expression in CD4 T cells (1997) Cell, 89, pp. 587-596 | ||
| 504 | |a Szabo, S.J., Kim, S.T., Costa, G.L., A novel transcription factor, T-bet, direct Th1 lineage commitment (2000) Cell, 100, pp. 655-669 | ||
| 504 | |a Grogan, J.L., Locksley, R.M., T helper cell differentiation: On again, off again (2002) Curr. Opin. Immunol., 14, pp. 366-372 | ||
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| 504 | |a Garcia, M.M., Kapcala, L.P., Growth of a microprolactinoma to a macroprolactinoma during estrogen therapy (1995) J. Endocrinol. Invest., 18, pp. 450-455 | ||
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| 504 | |a Paez Pereda, M., Giacomini, D., Refojo, D., Involvement of bone morphogenetic protein Y (BMP-Y) in pituitary prolactinoma pathogenesis through a SMAD/estrogen receptor crosstalk (2003) Proc. Natl. Acad. Sci. USA, 100, pp. 1034-1039 | ||
| 520 | 3 | |a An essential event in immune activation is the increase of cytokines in both plasma and immune tissues. Steroid hormones influence several adaptive responses in both health and disease. Cytokines and steroids have an intimate cross-communication in many systems, making possible a satisfactory adaptive response to environmental changes. The ultimate level of integration of the cytokine-steroids cross-talk is the molecular level. We have demonstrated this in four types of cross-talk mechanisms on different cells in which steroids have major roles: (1) The tumor necrosis factor (TNF)-glucocorticoid receptor (GR) transcriptional interaction in cellular targets of TNF-induced cytotoxicity. TNF potentiates the transactivation activity of GR and the priming with TNF increases the protective action of GR on TNF-induced cytotoxicity. (2) The GR-T cell receptor (TCR) antagonism in GR-TCR-induced T cell apoptosis and its modulation by cAMP. cAMP inhibits the TCR-induced apoptosis through a PKA-CREB-dependent mechanism and potentiates glucocorticoid-induced apoptosis by means of a CREB-independent mechanism. (3) The GR influence on Th1-Th2 cytokine expression and differentiation. Glucocorticoids inhibit the induction of GATA-3 and T-bet transcription factors. (4) The influence of ER/Smad-4 signaling cross-communication on prolactinoma pathogenesis. Physical and functional interactions between Smad-4 and estrogen receptors take place in prolactinoma cells, providing a molecular explanation to link the tumorigenic action of these two important players of prolactinoma pathogenesis. The molecular cross-talk between steroids and transcription factors is the mechanism that provides the basis for the outcome of adaptive responses integrating the systemic information provided by hormones and cytokines. |l eng | |
| 593 | |a Lab. de Fisiol. y Biol. Molecular, Depto. Fisiol. y Biol. Molec. y Cel., C1428EHA, Buenos Aires, Argentina | ||
| 593 | |a Max-Planck Institute of Psychiatry, 80804 Munich, Germany | ||
| 593 | |a Lab. Fisiol. y Biol. Molecular, FCEN-Universidad de Buenos Aires, Pabellón II (C1428EHA), Buenos Aires, Argentina | ||
| 690 | 1 | 0 | |a APOPTOSIS |
| 690 | 1 | 0 | |a BMP-4 |
| 690 | 1 | 0 | |a CAMP |
| 690 | 1 | 0 | |a ESTROGEN |
| 690 | 1 | 0 | |a GATA-3 |
| 690 | 1 | 0 | |a GLUCOCORTICOID |
| 690 | 1 | 0 | |a PROLACTINOMA |
| 690 | 1 | 0 | |a T CELL RECEPTOR (TCR) |
| 690 | 1 | 0 | |a T-BET |
| 690 | 1 | 0 | |a TH1-TH2 DIFFERENTIATION |
| 690 | 1 | 0 | |a TUMOR NECROSIS FACTOR (TNF) |
| 690 | 1 | 0 | |a CYCLIC AMP |
| 690 | 1 | 0 | |a CYCLIC AMP DEPENDENT PROTEIN KINASE |
| 690 | 1 | 0 | |a CYCLIC AMP RESPONSIVE ELEMENT BINDING PROTEIN |
| 690 | 1 | 0 | |a CYTOKINE |
| 690 | 1 | 0 | |a ESTROGEN |
| 690 | 1 | 0 | |a ESTROGEN RECEPTOR |
| 690 | 1 | 0 | |a GLUCOCORTICOID RECEPTOR |
| 690 | 1 | 0 | |a SMAD4 PROTEIN |
| 690 | 1 | 0 | |a STEROID HORMONE |
| 690 | 1 | 0 | |a STEROID RECEPTOR |
| 690 | 1 | 0 | |a T LYMPHOCYTE RECEPTOR |
| 690 | 1 | 0 | |a TRANSCRIPTION FACTOR |
| 690 | 1 | 0 | |a TRANSCRIPTION FACTOR GATA 3 |
| 690 | 1 | 0 | |a TUMOR NECROSIS FACTOR |
| 690 | 1 | 0 | |a ADAPTATION |
| 690 | 1 | 0 | |a APOPTOSIS |
| 690 | 1 | 0 | |a CARCINOGENESIS |
| 690 | 1 | 0 | |a CONFERENCE PAPER |
| 690 | 1 | 0 | |a CYTOKINE PRODUCTION |
| 690 | 1 | 0 | |a CYTOTOXICITY |
| 690 | 1 | 0 | |a GENETIC TRANSCRIPTION |
| 690 | 1 | 0 | |a IMMUNE RESPONSE |
| 690 | 1 | 0 | |a LYMPHOCYTE DIFFERENTIATION |
| 690 | 1 | 0 | |a PROLACTINOMA |
| 690 | 1 | 0 | |a PROTEIN PROTEIN INTERACTION |
| 690 | 1 | 0 | |a SIGNAL TRANSDUCTION |
| 690 | 1 | 0 | |a T LYMPHOCYTE |
| 690 | 1 | 0 | |a TARGET CELL |
| 690 | 1 | 0 | |a TH1 CELL |
| 690 | 1 | 0 | |a TH2 CELL |
| 690 | 1 | 0 | |a TRANSACTIVATION |
| 700 | 1 | |a Liberman, A.C. | |
| 700 | 1 | |a Giacomini, D. | |
| 700 | 1 | |a Nagashima, A.C. | |
| 700 | 1 | |a Graciarena, M. | |
| 700 | 1 | |a Echenique, C. | |
| 700 | 1 | |a Paez Pereda, M. | |
| 700 | 1 | |a Stalla, G. | |
| 700 | 1 | |a Holsboer, F. | |
| 700 | 1 | |a Arzt, E. | |
| 773 | 0 | |d New York Academy of Sciences, 2003 |g v. 992 |h pp. 196-204 |p Ann. New York Acad. Sci. |x 00778923 |w (AR-BaUEN)CENRE-1541 |t Annals of the New York Academy of Sciences | |
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