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. Author manuscript; available in PMC: 2009 Aug 15.
Published in final edited form as: Biol Psychiatry. 2008 Aug 15;64(4):263–265. doi: 10.1016/j.biopsych.2008.05.018

Figure 1. Tipping the Balance Toward NF-kB Signaling and Inflammation During Chronic Stress.

Figure 1

Increased inflammatory [nuclear factor kappa B (NFkB)] signaling during chronic stress may be a function of increased expression of NF-kB-linked toll-like receptors (TLRs) and/or increased production of innate immune cytokines associated with a decrease in glucocorticoid signaling secondary to decreased glucocorticoid receptor (GR) translocation, GR protein-protein interactions with other inflammatory signaling molecules or increased expression of the inert GR isoform, GR beta.