• Corpus ID: 22109868

Modulatory effects of glucocorticoids and catecholamines on human interleukin-12 and interleukin-10 production: clinical implications.

  title={Modulatory effects of glucocorticoids and catecholamines on human interleukin-12 and interleukin-10 production: clinical implications.},
  author={Ilia J. Elenkov and Dimitris A. Papanicolaou and Ronald L. Wilder and George P. Chrousos},
  journal={Proceedings of the Association of American Physicians},
  volume={108 5},
Interleukin-12 (IL-12) is a key inducer of differentiation of uncommitted T helper (TH) cells toward the TH1 phenotype, which regulates cellular immunity, whereas IL-10 inhibits TH1 functions and potentiates TH2-regulated responses (i.e., humoral immunity). To examine the potential effects of stress on TH1/TH2 balance, we studied the ability of three prototype stress hormones-dexamethasone (a synthetic glucocorticoid) and the catecholamines norepinephrine and epinephrine-to alter the production… 

Inhibition of Th1 Immune Response by Glucocorticoids: Dexamethasone Selectively Inhibits IL-12-Induced Stat4 Phosphorylation in T Lymphocytes1

Blocking IL-12-induced Stat4 phosphorylation appears to be a new suppressive action of glucocorticoids on the Th1 cellular immune response and may help explain the glucoc Corticoid-induced shift toward the Th2 humoral immune response.

Neuroendocrine Regulation of IL‐12 and TNF‐α/IL‐10 Balance: Clinical Implications

Better understanding of the neuroendocrine regulation of IL‐12, TNF‐α/IL‐10 balance might help the development of new therapeutic strategies for the treatment of Th1‐ and Th2‐mediated human diseases.

Beta-adrenergic modulation of human type-1/type-2 cytokine balance.

Histamine potently suppresses human IL-12 and stimulates IL-10 production via H2 receptors.

It is reported that histamine dose-dependently inhibited the secretion of human IL-12 and increased the production of IL-10 in LPS-stimulated whole blood cultures and may represent a novel mechanism by which excessive secretion of histamine potentiates Th2-mediated allergic reactions and contributes to the development of certain infections and tumors normally eliminated by Th1-dependent immune mechanisms.

An alternate mechanism of glucocorticoid anti‐proliferative effect: promotion of a Th2 cytokine‐secreting profile

Collectively, this indicates that, in exerting their anti‐proliferative effects, GCs act indirectly by altering Th1/Th2 cytokine balance, blocking the (pro‐ inflammatory) Th1 program and favoring the (anti‐inflammatory) Th2 program.

Norepinephrine accelerates HIV replication via protein kinase A-dependent effects on cytokine production.

PKA-dependent suppression of cytokine production appears to mediate the enhancement of HIV-1 replication by NE, indicating transduction via the adrenoreceptor signaling pathway.