 | NEUROENDOCRINE AND NEURAL REGULATION OF AUTOIMMUNE AND INFLAMMATORY DISEASE: Molecular, Systems, and Clinical Insights
Copyright © 2003 by the New York Academy of Sciences
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Annals of the New York Academy of Sciences 992:196-204 (2003)
© 2003 New York Academy of Sciences
Integrating Systemic Information at the Molecular Level
Cross-Talk between Steroid Receptors and Cytokine Signaling on Different Target Cells
DAMIÁN REFOJOa,b,
ANA C. LIBERMANa,b,
DAMIANA GIACOMINIa,
ALBERTO CARBIA NAGASHIMAa,b,
MARIANA GRACIARENAa,
CARLOS ECHENIQUEa,
MARCELO PAEZ PEREDAc,
GÜNTER STALLAc,
FLORIAN HOLSBOERc AND
EDUARDO ARZTa,b
aLaboratorio de Fisiología y Biología Molecular, Departamento de Fisiología y Biología Molecular y Celular, Facultad de Ciencias Exactas y Naturales (FCEN), Universidad de Buenos Aires, Ciudad Universitaria, Pabellón II, C1428EHA, Buenos Aires, Argentina
bMembers of the Argentine National Research Council (CONICET)
cMax-Planck Institute of Psychiatry, 80804 Munich, Germany
Address for correspondence: Dr. Eduardo Arzt, Lab Fisiología y Biología Molecular, FCEN-Universidad de Buenos Aires, Cuidad Universitaria, Pabellón II (C1428EHA), Buenos Aires, Argentina. Voice: 54-11-4576-3368; fax: 54-11-4576-3321.
earzt{at}fbmc.fcen.uba.ar.
Ann. N.Y. Acad. Sci. 922: 196-204 (2003).
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.
Key Words: glucocorticoid • tumor necrosis factor (TNF) • cAMP • T cell receptor (TCR) • apoptosis • GATA-3 • T-bet • Th1-Th2 differentiation • BMP-4 • prolactinoma • estrogen
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