Immune responses are highly could we say receptive to endocrine molecules mainly due to the vast expression of hormone receptors on myeloid and lymphoid cell lineages. The endocrine milieu may regulate B and T cell responsiveness. Sex hormones execute several actions on T cells under physiological processes of non-reproductive tissues. Currently, it is known that multiple factors are involved in the onset of autoimmune diseases including genetic, environmental, and endocrine compounds that promote greater susceptibility but are not determinant individually for setting autoimmunity. Differences in the incidence of autoimmune diseases in females compared to males clearly demonstrates that female hormonal homeostasis, and biology linked to this, such as XX chromosomes and sexual differentiation, are very important risk factors. Experimental models for autoimmune diseases have shown a marked pro-inflammatory role for certain hormonal factors and their receptors such as Estrogen Receptor (ER), Progesterone Receptor (PR), Glucocorticoid Receptor (GR) and (Prolactin receptor )PRL-r, and that this can contribute to disease development. Estrogen and prolactin exert mostly stimulatory functions of immune cells, promoting activation and autoimmunity. In contrast, progesterone is mainly suppressive, repressing autoimmunity and most importantly, favoring embryo implantation by the maternal immune system. However, in some physiological situations such as mammary gland function during lactation, there are some instances in which the effect of regulation of hormone secretion and actions remain unclear. Further, the role of many other endocrine factors, such as thyroid hormones (THs) receptors (THR), dopamine receptors, and adrenergic receptors, have been barely addressed and could play a role in modulating different immune cells. Dendritic cells express receptors for triiodothyronine (T3) which may promote maturation, increase phagocytic activity, cytokine production and T cell priming. Additionally, thyroxine may influence macrophage migration, through the action of these hormones in macrophage inhibitory factor and ROS production. Deciphering the effects of multi-faceted hormones on the immunity of B and T cells could be critical in understand key pathogenic mechanisms and designing new strategies for immune mediated diseases.
This Research Topic is aiming to shed light on how the endocrine milieu, endocrine disruptors, endocrine genes, and stress may modulate T cell biology with the main focus being on how T cell-mediated autoimmune responses may be affected by endocrine disruptors.
We welcome the submission of Original and Review articles addressing the scope of this collection, where endocrine modulation of T and B cells are highlighted. Topics may include, but are not limited to:
• Epigenetic profiling of endocrine genes in immune cells
• Thyroid hormones and immune homeostasis
• Effect of Sex-Steroids (Estrogens, Progesterone and Androgens) on T and B cell biology
• Stress response and glucocorticoids
• PRL, GH and Glucocorticoids
• Homeostasis functions of T cells during development
• Immune changes during gestation and lactation
Immune responses are highly could we say receptive to endocrine molecules mainly due to the vast expression of hormone receptors on myeloid and lymphoid cell lineages. The endocrine milieu may regulate B and T cell responsiveness. Sex hormones execute several actions on T cells under physiological processes of non-reproductive tissues. Currently, it is known that multiple factors are involved in the onset of autoimmune diseases including genetic, environmental, and endocrine compounds that promote greater susceptibility but are not determinant individually for setting autoimmunity. Differences in the incidence of autoimmune diseases in females compared to males clearly demonstrates that female hormonal homeostasis, and biology linked to this, such as XX chromosomes and sexual differentiation, are very important risk factors. Experimental models for autoimmune diseases have shown a marked pro-inflammatory role for certain hormonal factors and their receptors such as Estrogen Receptor (ER), Progesterone Receptor (PR), Glucocorticoid Receptor (GR) and (Prolactin receptor )PRL-r, and that this can contribute to disease development. Estrogen and prolactin exert mostly stimulatory functions of immune cells, promoting activation and autoimmunity. In contrast, progesterone is mainly suppressive, repressing autoimmunity and most importantly, favoring embryo implantation by the maternal immune system. However, in some physiological situations such as mammary gland function during lactation, there are some instances in which the effect of regulation of hormone secretion and actions remain unclear. Further, the role of many other endocrine factors, such as thyroid hormones (THs) receptors (THR), dopamine receptors, and adrenergic receptors, have been barely addressed and could play a role in modulating different immune cells. Dendritic cells express receptors for triiodothyronine (T3) which may promote maturation, increase phagocytic activity, cytokine production and T cell priming. Additionally, thyroxine may influence macrophage migration, through the action of these hormones in macrophage inhibitory factor and ROS production. Deciphering the effects of multi-faceted hormones on the immunity of B and T cells could be critical in understand key pathogenic mechanisms and designing new strategies for immune mediated diseases.
This Research Topic is aiming to shed light on how the endocrine milieu, endocrine disruptors, endocrine genes, and stress may modulate T cell biology with the main focus being on how T cell-mediated autoimmune responses may be affected by endocrine disruptors.
We welcome the submission of Original and Review articles addressing the scope of this collection, where endocrine modulation of T and B cells are highlighted. Topics may include, but are not limited to:
• Epigenetic profiling of endocrine genes in immune cells
• Thyroid hormones and immune homeostasis
• Effect of Sex-Steroids (Estrogens, Progesterone and Androgens) on T and B cell biology
• Stress response and glucocorticoids
• PRL, GH and Glucocorticoids
• Homeostasis functions of T cells during development
• Immune changes during gestation and lactation
