Figure 3. Signaling molecules involved in regulating stress-related neuroinflammation. Neuroimmune signaling molecules that control inflammatory response can be categorized into three types, as follows: (i) host-derived danger, damage, and disease signals—including cytokines, chemokines, and damage-associated molecular patterns (DAMPS)—that acutely activate inflammatory signaling pathways; (ii) rapid neural signals, such as norepinephrine and glutamate, that rapidly drive the stress response and cytokine production throughout the body; and (iii) neuroendocrine signals, particularly corticosteroids and progesterone, which may serve to constrain the inflammatory process and dampen production of inflammatory factors. AP-1 , activator protein 1 ; ATP, adenosine triphosphate; AR, adrenergic receptor; cAMP, cyclic adenosine monophosphate; CRE, cAMP-response element; CREB, cAMP-response-element binding protein; DAMPs, damage-associated molecular patterns; ERK, extracellular-signal-regulated kinase; GR, glucocorticoid receptor; HMGB1, high-mobility group box 1 ; HSPs, heat shock proteins; ICE, interleukin-1 -converting enzyme; IL, interleukin; MAPK, mitogen-activated protein kinase; MyD88, myeloid differentiation primary response gene 88; NFkB, nuclear factor kB; nGRE, negative glucocorticoid response element; NMDAR, N-methyl-d-aspartate receptor; PKA, protein kinase A; PKC, protein kinase C; TNF, tumor necrosis factor; TLR, Toll-like receptor; TRAF6, TNF receptor-associated factor 6.