We have mentioned in this blog that, in the inflammatory process, there are molecules called cytokines that promote inflammation (proinflammatory) and molecules that inhibit inflammation (anti-inflammatory). The interaction between both modulates the result of the inflammatory process. Certain chronic diseases are characterized by the persistence of inflammation because among other factors the activity of the proinflammatory cytokines predominates, which leads to chronic inflammation.
When we read articles related to these topics, two terms often appear that, because they have a certain time in circulation, are no longer explained. I will briefly refer to NF-ƙB and SOCS.
NF-ƙB: Activated B cell-facilitating light chain kappa factor. Proinflammatory cytokines activate this factor to fulfill their function. This protein is usually interpreted as the "master switch" for the activation of transcription of proinflammatory molecules (1).
SOCS: Suppressor of cytokine signaling. Anti-inflammatory cotokines often promote SOCS, which bind to the cytoplasmic half of the receptor protein of other signaling cytokines, suppressing its effect (1).
In this case, the anti-inflammatory cytokines restrain the proinflammatory cells by activating SOCS.
(1) Tousolis et al. The role and predictive value of cytokines in atherosclerosis and coronary artery disease. Current Medicinal Chemistry 2015 (22): 2636-50.