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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todo:paper_00778923_v992_n_p196_Refojo2023-10-03T14:54:24Z Integrating systemic information at the molecular level: Cross-talk between steroid receptors and cytokine signaling on different target cells Refojo, D. Liberman, A.C. Giacomini, D. Nagashima, A.C. Graciarena, M. Echenique, C. Paez Pereda, M. Stalla, G. Holsboer, F. Arzt, E. Apoptosis BMP-4 cAMP Estrogen GATA-3 Glucocorticoid Prolactinoma T cell receptor (TCR) T-bet Th1-Th2 differentiation Tumor necrosis factor (TNF) cyclic AMP cyclic AMP dependent protein kinase cyclic AMP responsive element binding protein cytokine estrogen estrogen receptor glucocorticoid receptor Smad4 protein steroid hormone steroid receptor T lymphocyte receptor transcription factor transcription factor GATA 3 tumor necrosis factor adaptation apoptosis carcinogenesis conference paper cytokine production cytotoxicity genetic transcription immune response lymphocyte differentiation prolactinoma protein protein interaction signal transduction T lymphocyte target cell Th1 cell Th2 cell transactivation 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. Fil:Refojo, D. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Liberman, A.C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Giacomini, D. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Graciarena, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Paez Pereda, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. SER info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_00778923_v992_n_p196_Refojo |
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Universidad de Buenos Aires |
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I-28 |
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R-134 |
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Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
Apoptosis BMP-4 cAMP Estrogen GATA-3 Glucocorticoid Prolactinoma T cell receptor (TCR) T-bet Th1-Th2 differentiation Tumor necrosis factor (TNF) cyclic AMP cyclic AMP dependent protein kinase cyclic AMP responsive element binding protein cytokine estrogen estrogen receptor glucocorticoid receptor Smad4 protein steroid hormone steroid receptor T lymphocyte receptor transcription factor transcription factor GATA 3 tumor necrosis factor adaptation apoptosis carcinogenesis conference paper cytokine production cytotoxicity genetic transcription immune response lymphocyte differentiation prolactinoma protein protein interaction signal transduction T lymphocyte target cell Th1 cell Th2 cell transactivation |
| spellingShingle |
Apoptosis BMP-4 cAMP Estrogen GATA-3 Glucocorticoid Prolactinoma T cell receptor (TCR) T-bet Th1-Th2 differentiation Tumor necrosis factor (TNF) cyclic AMP cyclic AMP dependent protein kinase cyclic AMP responsive element binding protein cytokine estrogen estrogen receptor glucocorticoid receptor Smad4 protein steroid hormone steroid receptor T lymphocyte receptor transcription factor transcription factor GATA 3 tumor necrosis factor adaptation apoptosis carcinogenesis conference paper cytokine production cytotoxicity genetic transcription immune response lymphocyte differentiation prolactinoma protein protein interaction signal transduction T lymphocyte target cell Th1 cell Th2 cell transactivation Refojo, D. Liberman, A.C. Giacomini, D. Nagashima, A.C. Graciarena, M. Echenique, C. Paez Pereda, M. Stalla, G. Holsboer, F. Arzt, E. Integrating systemic information at the molecular level: Cross-talk between steroid receptors and cytokine signaling on different target cells |
| topic_facet |
Apoptosis BMP-4 cAMP Estrogen GATA-3 Glucocorticoid Prolactinoma T cell receptor (TCR) T-bet Th1-Th2 differentiation Tumor necrosis factor (TNF) cyclic AMP cyclic AMP dependent protein kinase cyclic AMP responsive element binding protein cytokine estrogen estrogen receptor glucocorticoid receptor Smad4 protein steroid hormone steroid receptor T lymphocyte receptor transcription factor transcription factor GATA 3 tumor necrosis factor adaptation apoptosis carcinogenesis conference paper cytokine production cytotoxicity genetic transcription immune response lymphocyte differentiation prolactinoma protein protein interaction signal transduction T lymphocyte target cell Th1 cell Th2 cell transactivation |
| description |
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. |
| format |
SER |
| author |
Refojo, D. Liberman, A.C. Giacomini, D. Nagashima, A.C. Graciarena, M. Echenique, C. Paez Pereda, M. Stalla, G. Holsboer, F. Arzt, E. |
| author_facet |
Refojo, D. Liberman, A.C. Giacomini, D. Nagashima, A.C. Graciarena, M. Echenique, C. Paez Pereda, M. Stalla, G. Holsboer, F. Arzt, E. |
| author_sort |
Refojo, D. |
| title |
Integrating systemic information at the molecular level: Cross-talk between steroid receptors and cytokine signaling on different target cells |
| title_short |
Integrating systemic information at the molecular level: Cross-talk between steroid receptors and cytokine signaling on different target cells |
| title_full |
Integrating systemic information at the molecular level: Cross-talk between steroid receptors and cytokine signaling on different target cells |
| title_fullStr |
Integrating systemic information at the molecular level: Cross-talk between steroid receptors and cytokine signaling on different target cells |
| title_full_unstemmed |
Integrating systemic information at the molecular level: Cross-talk between steroid receptors and cytokine signaling on different target cells |
| title_sort |
integrating systemic information at the molecular level: cross-talk between steroid receptors and cytokine signaling on different target cells |
| url |
http://hdl.handle.net/20.500.12110/paper_00778923_v992_n_p196_Refojo |
| work_keys_str_mv |
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1807318251414224896 |