INVESTIGADORES
GENARO Ana Maria
artículos
Título:
Immune System Modulation by Thyroid Axis Includes Direct
Autor/es:
MARÍA LAURA BARREIRO ARCOS; ALICIA JUANA KLECHA; ANA MARÍA GENARO; GRACIELA ALICIA CREMASCHI
Revista:
Immun. Endoc. Metab. Agents in Med. Chem
Editorial:
Bentham Science Publishers
Referencias:
Año: 2010 vol. 10 p. 1 - 10
ISSN:
1871-5222
Resumen:
A bidirectional circuit exists between the neuroendocrine and immune systems that functions to
maintain and protect the internal homeostasis of the organism. In this context, interactions between thyroid
hormones (TH) and the immune system are revealed mainly by the presence of specific receptors for TH on
lymphocytes or by the frequent immune alterations associated with physiological or pathological fluctuations
of TH. In this context, both hypothyroidism in humans and experimentally-induced hypothyroidism in rodents
have been shown to diminish thymus activity, to lead to spleen and lymph node involution and to depress
humoral and cell-mediated immune responses. All these effects are reversed by restoration of the euthyroid
state. In contrast, in vivo up-regulation of TH levels, but not those of thyrotropic hormones, leads to an
increase in lymphocyte reactivity and an increment of inflammatory and T-cell derived cytokines.
Additionally, TH direct actions on T lymphocytes were recently demonstrated as well, showing that TH are
able to increase T cell proliferation through the activation of both nongenomic and genomic intracellular
signals. These actions point to the important role that these hormones play in regulating lymphocyte function.
Additional studies are needed of the mechanisms involved in cellular interactions within the
immunoneuroendocrine network, as well as the consequences of their alterations. Such studies may disclose
contributions of TH to the pathophysiology of the immune system and thus suggest novel approaches to
modulation of immunopathology via manipulation of endogenous TH.
increase in lymphocyte reactivity and an increment of inflammatory and T-cell derived cytokines.
Additionally, TH direct actions on T lymphocytes were recently demonstrated as well, showing that TH are
able to increase T cell proliferation through the activation of both nongenomic and genomic intracellular
signals. These actions point to the important role that these hormones play in regulating lymphocyte function.
Additional studies are needed of the mechanisms involved in cellular interactions within the
immunoneuroendocrine network, as well as the consequences of their alterations. Such studies may disclose
contributions of TH to the pathophysiology of the immune system and thus suggest novel approaches to
modulation of immunopathology via manipulation of endogenous TH.
have been shown to diminish thymus activity, to lead to spleen and lymph node involution and to depress
humoral and cell-mediated immune responses. All these effects are reversed by restoration of the euthyroid
state. In contrast, in vivo up-regulation of TH levels, but not those of thyrotropic hormones, leads to an
increase in lymphocyte reactivity and an increment of inflammatory and T-cell derived cytokines.
Additionally, TH direct actions on T lymphocytes were recently demonstrated as well, showing that TH are
able to increase T cell proliferation through the activation of both nongenomic and genomic intracellular
signals. These actions point to the important role that these hormones play in regulating lymphocyte function.
Additional studies are needed of the mechanisms involved in cellular interactions within the
immunoneuroendocrine network, as well as the consequences of their alterations. Such studies may disclose
contributions of TH to the pathophysiology of the immune system and thus suggest novel approaches to
modulation of immunopathology via manipulation of endogenous TH.
increase in lymphocyte reactivity and an increment of inflammatory and T-cell derived cytokines.
Additionally, TH direct actions on T lymphocytes were recently demonstrated as well, showing that TH are
able to increase T cell proliferation through the activation of both nongenomic and genomic intracellular
signals. These actions point to the important role that these hormones play in regulating lymphocyte function.
Additional studies are needed of the mechanisms involved in cellular interactions within the
immunoneuroendocrine network, as well as the consequences of their alterations. Such studies may disclose
contributions of TH to the pathophysiology of the immune system and thus suggest novel approaches to
modulation of immunopathology via manipulation of endogenous TH.
. In this context, both hypothyroidism in humans and experimentally-induced hypothyroidism in rodents
have been shown to diminish thymus activity, to lead to spleen and lymph node involution and to depress
humoral and cell-mediated immune responses. All these effects are reversed by restoration of the euthyroid
state. In contrast, in vivo up-regulation of TH levels, but not those of thyrotropic hormones, leads to an
increase in lymphocyte reactivity and an increment of inflammatory and T-cell derived cytokines.
Additionally, TH direct actions on T lymphocytes were recently demonstrated as well, showing that TH are
able to increase T cell proliferation through the activation of both nongenomic and genomic intracellular
signals. These actions point to the important role that these hormones play in regulating lymphocyte function.
Additional studies are needed of the mechanisms involved in cellular interactions within the
immunoneuroendocrine network, as well as the consequences of their alterations. Such studies may disclose
contributions of TH to the pathophysiology of the immune system and thus suggest novel approaches to
modulation of immunopathology via manipulation of endogenous TH.
increase in lymphocyte reactivity and an increment of inflammatory and T-cell derived cytokines.
Additionally, TH direct actions on T lymphocytes were recently demonstrated as well, showing that TH are
able to increase T cell proliferation through the activation of both nongenomic and genomic intracellular
signals. These actions point to the important role that these hormones play in regulating lymphocyte function.
Additional studies are needed of the mechanisms involved in cellular interactions within the
immunoneuroendocrine network, as well as the consequences of their alterations. Such studies may disclose
contributions of TH to the pathophysiology of the immune system and thus suggest novel approaches to
modulation of immunopathology via manipulation of endogenous TH.
in vivo up-regulation of TH levels, but not those of thyrotropic hormones, leads to an
increase in lymphocyte reactivity and an increment of inflammatory and T-cell derived cytokines.
Additionally, TH direct actions on T lymphocytes were recently demonstrated as well, showing that TH are
able to increase T cell proliferation through the activation of both nongenomic and genomic intracellular
signals. These actions point to the important role that these hormones play in regulating lymphocyte function.
Additional studies are needed of the mechanisms involved in cellular interactions within the
immunoneuroendocrine network, as well as the consequences of their alterations. Such studies may disclose
contributions of TH to the pathophysiology of the immune system and thus suggest novel approaches to
modulation of immunopathology via manipulation of endogenous TH.via manipulation of endogenous TH.