That the central nervous system (CNS) and the immune system (Image ) communicate has always been regarded with a sort of suspicion, especially by immunologists, already happy with the large array of internal mechanisms governing the immune response. It is undeniable, however, that the IS, when faced with immunological attacks, can send signals to the CNS that result in changes in behavior and, through the hypothalamic-pituitary-adrenal axis (HPPA), to glucocorticoid-mediated inhibition of the immune response. Indeed, experimental animal models have long existed that prove that disruption of this axis can lead to misfunction of the immune system, particularly in autoimmune diseases. Either non-cognitive (immune) or cognitive (i.e. psychological) stress can thus modulate the function of these cells. Changes in humans are not so quick to be understood as those in animals. However, a sufficient body of data has accumulated so far to demonstrate that changes in the sex hormones to which individuals are exposed in their life have a strong impact on immune function. This is evident when considering autoimmune diseases, which already present with a marked dimorphism and whose incidence or clinical course seems to be marked by the hormonal changes occurring during a woman’s life, estrogens being the more implicated hormones. A breakthrough in the understanding of how hormones can modulate the IS has come from the observation that pituitary hormones functionally linked to estrogens, such as PRL, activate signaling pathways common to cytokine receptors. In addition, the cytokine genes themselves are targets for hormone action and dictate whether a T lymphocyte response will predominantly be of the cellular (Th1) or the humoral (Th2) type. Deviation in the Th1/Th2 balance is a consistent feature of autoimmunity and of immune anergy observed in some infectious diseases and in cancer. The possibility offered by signaling transduction studies of dissecting the molecular steps leading to activation of target genes is now providing an explanation to the long-known opposing action of HPAA-prototype (GC) and pituitary-prototype (PRL, GH) hormones. Control of the immune response can be attained by the alternate silencing/activation of these major players in the fine-tuned regulation of the IS.
Communication of the central nervous and the immune systems.
MATERA, Lina;
2000-01-01
Abstract
That the central nervous system (CNS) and the immune system (Image ) communicate has always been regarded with a sort of suspicion, especially by immunologists, already happy with the large array of internal mechanisms governing the immune response. It is undeniable, however, that the IS, when faced with immunological attacks, can send signals to the CNS that result in changes in behavior and, through the hypothalamic-pituitary-adrenal axis (HPPA), to glucocorticoid-mediated inhibition of the immune response. Indeed, experimental animal models have long existed that prove that disruption of this axis can lead to misfunction of the immune system, particularly in autoimmune diseases. Either non-cognitive (immune) or cognitive (i.e. psychological) stress can thus modulate the function of these cells. Changes in humans are not so quick to be understood as those in animals. However, a sufficient body of data has accumulated so far to demonstrate that changes in the sex hormones to which individuals are exposed in their life have a strong impact on immune function. This is evident when considering autoimmune diseases, which already present with a marked dimorphism and whose incidence or clinical course seems to be marked by the hormonal changes occurring during a woman’s life, estrogens being the more implicated hormones. A breakthrough in the understanding of how hormones can modulate the IS has come from the observation that pituitary hormones functionally linked to estrogens, such as PRL, activate signaling pathways common to cytokine receptors. In addition, the cytokine genes themselves are targets for hormone action and dictate whether a T lymphocyte response will predominantly be of the cellular (Th1) or the humoral (Th2) type. Deviation in the Th1/Th2 balance is a consistent feature of autoimmunity and of immune anergy observed in some infectious diseases and in cancer. The possibility offered by signaling transduction studies of dissecting the molecular steps leading to activation of target genes is now providing an explanation to the long-known opposing action of HPAA-prototype (GC) and pituitary-prototype (PRL, GH) hormones. Control of the immune response can be attained by the alternate silencing/activation of these major players in the fine-tuned regulation of the IS.
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