The sympathetic nerve--an integrative interface between two supersystems: the brain and the immune system.
- I. Elenkov, R. Wilder, G. Chrousos, E. Vizi
- BiologyPharmacological Reviews
- 1 December 2000
The activation of SNS during an immune response might be aimed to localize the inflammatory response, through induction of neutrophil accumulation and stimulation of more specific humoral immune responses, although systemically it may suppress Th1 responses, and, thus protect the organism from the detrimental effects of proinflammatory cytokines and other products of activated macrophages.
Stress Hormones, Th1/Th2 patterns, Pro/Anti-inflammatory Cytokines and Susceptibility to Disease
- I. Elenkov, G. Chrousos
- Biology, MedicineTrends in endocrinology and metabolism
- 1 November 1999
Stress Hormones, Proinflammatory and Antiinflammatory Cytokines, and Autoimmunity
- I. Elenkov, G. Chrousos
- BiologyAnnals of the New York Academy of Sciences
- 1 June 2002
Excessive immune response, through activation of the stress system, stimulates an important negative feedback mechanism, which protects the organism from an “overshoot” of proinflammatory cytokines and other products of activated macrophages with tissue‐damaging potential.
Glucocorticoids and the Th1/Th2 Balance
- I. Elenkov
- Biology, MedicineAnnals of the New York Academy of Sciences
- 1 June 2004
During an immune response and inflammation, the activation of the stress system, and thus increased levels of systemic GCs through induction of a Th2 shift, may actually protect the organism from systemic “overshooting” with Th1/pro‐inflammatory cytokines and other products of activated macrophages with tissue‐damaging potential.
Stress System Activity, Innate and T Helper Cytokines, and Susceptibility to Immune‐Related Diseases
- Emanuele Calcagni, I. Elenkov
- Biology, MedicineAnnals of the New York Academy of Sciences
- 1 June 2006
Stress hormones‐induced inhibition or upregulation of innate and Th cytokine production may represent an important mechanism by which stress affects disease susceptibility, activity, and outcome of various immune‐related diseases.
Histamine potently suppresses human IL-12 and stimulates IL-10 production via H2 receptors.
- I. Elenkov, E. Webster, D. Papanicolaou, T. Fleisher, G. Chrousos, R. Wilder
- Biology, MedicineJournal of Immunology
- 1 September 1998
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.
Cytokine Dysregulation, Inflammation and Well-Being
- I. Elenkov, D. Iezzoni, A. Daly, A. Harris, G. Chrousos
- Biology, MedicineNeuroimmunomodulation
- 1 September 2005
A dysfunctional neuroendocrine-immune interface associated with abnormalities of the ‘systemic anti-inflammatory feedback’ and/or ‘hyperactivity’ of the local pro-inflammatory factors may play a role in the pathogenesis of atopic/allergic and autoimmune diseases, obesity, depression, and atherosclerosis.
Neurohormonal-cytokine interactions: Implications for inflammation, common human diseases and well-being
- I. Elenkov
- Biology, MedicineNeurochemistry International
- 31 January 2008
Modulatory effects of glucocorticoids and catecholamines on human interleukin-12 and interleukin-10 production: clinical implications.
- I. Elenkov, D. Papanicolaou, R. Wilder, G. Chrousos
- Biology, MedicineProceedings of the Association of American…
- 1 September 1996
It is suggested that the central nervous system may regulate IL-12 and IL-10 secretion and, hence, TH1/TH2 balance via the peripheral end-effectors of the stress system, which may cause a selective suppression of TH1 functions and a shift toward a TH2 cytokine pattern rather than generalized TH suppression.
Ligand-Activation of the Adenosine A2a Receptors Inhibits IL-12 Production by Human Monocytes
- A. Link, T. Kino, I. Elenkov
- Biology, ChemistryJournal of Immunology
- 1 January 2000
Ligand activation of A2a receptors simultaneously inhibits IL-12 and stimulates IL-10 production by human monocytes, and through this mechanism, ADO released in excess during inflammatory and ischemic conditions, or tissue injury, may contribute to selective suppression of Th1 responses and cellular immunity.
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