Article date: July 1999
By: György Haskó, Csaba Szabó, in Volume 127, Issue 6, pages 1295-1304
Interleukin‐12 (IL‐12) is a pivotal cytokine in driving the immune system towards a T helper (Th)1 type response and preventing a Th2 type immune profile. Therefore, IL‐12 is indispensable in the defense against certain, mainly intracellular pathogens, but overproduction of this cytokine is crucially involved in the etiology of several inflammatory and autoimmune diseases.
Hence, IL‐12 is an ideal target for pharmacological intervention in the therapy of autoimmune and inflammatory diseases.
The production of IL‐12 and a resultant Th1 type immune response can be suppressed with several pharmacological approaches including modulation of intracellular cyclic AMP levels, glucocorticoids and nuclear factor‐κB inhibition. IL‐12 responsiveness may be inhibited using anti‐IL‐12 antibodies, soluble IL‐12 receptors or the IL‐12 p40 homodimer.
Exploitation of these approaches may provide novel means for the experimental therapy of a variety of pathophysiological states.
Interleukin‐12 (IL‐12) is a pivotal cytokine in driving the immune system towards a T helper (Th)1 type response and preventing a Th2 type immune profile. Therefore, IL‐12 is indispensable in the defense against certain, mainly intracellular pathogens, but overproduction of this cytokine is crucially involved in the etiology of several inflammatory and autoimmune diseases.
Hence, IL‐12 is an ideal target for pharmacological intervention in the therapy of autoimmune and inflammatory diseases.
The production of IL‐12 and a resultant Th1 type immune response can be suppressed with several pharmacological approaches including modulation of intracellular cyclic AMP levels, glucocorticoids and nuclear factor‐κB inhibition. IL‐12 responsiveness may be inhibited using anti‐IL‐12 antibodies, soluble IL‐12 receptors or the IL‐12 p40 homodimer.
Exploitation of these approaches may provide novel means for the experimental therapy of a variety of pathophysiological states.
British Journal of Pharmacology (1999) 127, 1295–1304; doi:10.1038/sj.bjp.0702689
DOI: 10.1038/sj.bjp.0702689
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