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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Sex hormone signaling and regulation of immune function
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<blockquote data-quote="madman" data-source="post: 269717" data-attributes="member: 13851"><p><strong>Figure 2. Estrogen and androgen signaling pathways in innate and adaptive immune cells</strong></p><p><strong></strong></p><p><strong>(A)</strong> Estrogens, including 17b-estradiol (E2), can bind to both intracellular (i.e., genomic) and membrane-bound (i.e., nongenomic) estrogen receptors (ERs) to cause transcriptional changes in immune cells.</p><p></p><p><strong>(B)</strong> E2 bound to genomic ERs translocates to the nucleus of macrophages to bind to estrogen response elements (EREs) on the genes that encode for several inflammatory and anti-inflammatory proteins, which can, for example, increase the secretion of IL-10 and promote an anti-inflammatory phenotype.</p><p></p><p><strong>(C)</strong> Genomic ER signaling in dendritic cells, follicular helper T cells, and B cells regulate coreceptor engagement, cytokine production, and activation of genes that encode for the proteins(e.g., TLR7 and AID) that underlie class-switch recombination and somatic hypermutations to regulate the antibody repertoire, which in mice can alter the ratio of IgG subclasses.</p><p></p><p><strong>(D)</strong> Androgens, including testosterone (T), can bind to either intracellular (i.e., genomic and nongenomic) and membrane-bound androgen receptors (ARs) to regulate activity in immune cells.</p><p></p><p><strong>(E) </strong>Testosterone (T), for example, can bind to ARsin neutrophils, NK cells, and tumor cells. The activation of ARs and binding to androgen response elements (AREs) on genes (e.g., IFN-g)in NK cells upregulates the expression of immunoregulatory receptors (e.g., PD-1) as well as reduces cytokine production, cytotoxic activity, and killing of tumor cells.</p><p></p><p><strong>(F)</strong> Intracellular AR signaling in CD8+ T cells can repress IFN-g and granzyme B activation and promote markers of exhaustion. In CD4+ T cells,T binding to intracellular ARs cause the ARcomplex to translocate to the nucleus, and bind to AREs on genes that repress differentiation into Th1, Th2, and Th17 subtypes.</p><p>[ATTACH=full]39168[/ATTACH]</p><p>[ATTACH=full]39169[/ATTACH]</p></blockquote><p></p>
[QUOTE="madman, post: 269717, member: 13851"] [B]Figure 2. Estrogen and androgen signaling pathways in innate and adaptive immune cells (A)[/B] Estrogens, including 17b-estradiol (E2), can bind to both intracellular (i.e., genomic) and membrane-bound (i.e., nongenomic) estrogen receptors (ERs) to cause transcriptional changes in immune cells. [B](B)[/B] E2 bound to genomic ERs translocates to the nucleus of macrophages to bind to estrogen response elements (EREs) on the genes that encode for several inflammatory and anti-inflammatory proteins, which can, for example, increase the secretion of IL-10 and promote an anti-inflammatory phenotype. [B](C)[/B] Genomic ER signaling in dendritic cells, follicular helper T cells, and B cells regulate coreceptor engagement, cytokine production, and activation of genes that encode for the proteins(e.g., TLR7 and AID) that underlie class-switch recombination and somatic hypermutations to regulate the antibody repertoire, which in mice can alter the ratio of IgG subclasses. [B](D)[/B] Androgens, including testosterone (T), can bind to either intracellular (i.e., genomic and nongenomic) and membrane-bound androgen receptors (ARs) to regulate activity in immune cells. [B](E) [/B]Testosterone (T), for example, can bind to ARsin neutrophils, NK cells, and tumor cells. The activation of ARs and binding to androgen response elements (AREs) on genes (e.g., IFN-g)in NK cells upregulates the expression of immunoregulatory receptors (e.g., PD-1) as well as reduces cytokine production, cytotoxic activity, and killing of tumor cells. [B](F)[/B] Intracellular AR signaling in CD8+ T cells can repress IFN-g and granzyme B activation and promote markers of exhaustion. In CD4+ T cells,T binding to intracellular ARs cause the ARcomplex to translocate to the nucleus, and bind to AREs on genes that repress differentiation into Th1, Th2, and Th17 subtypes. [ATTACH type="full"]39168[/ATTACH] [ATTACH type="full"]39169[/ATTACH] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Sex hormone signaling and regulation of immune function
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