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EP300 and PCAF also regulate inflammatory responses through their regulation of cyclooxygenase-2 (COX2) expression.
Endogenous release of adenosine triphosphate (ATP) in the liver activates purinergic P2 receptors (P2R), which regulate inflammatory responses, but little is known about the roles of these processes in the development of acute hepatitis.
This may have important implications in vivo since TGF-β and IL-10 regulate inflammatory responses.
These cells, originally identified in tumor bearing hosts, have been shown to possess potent suppressive functions and regulate inflammatory responses [24], [25].
The healthy gut is able to regulate inflammatory responses to commensal bacteria and food antigens whilst maintaining the capacity to respond to pathogens [1], [2], [3].
These proteins can regulate inflammatory responses by recruiting lymphocytes and monocytes/macrophages to areas of inflammation within the brain contributing to the injury and eventual loss of neurons [46], [47].
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Monocytes or macrophages, for instance, upregulate anti-inflammatory SH2-containing inositol phosphatase-1 (SHIP1) and regulate inflammatory response.
Regulatory T cells (Tregs) are known to regulate inflammatory response and suppress alloreactive T cells; the exact mechanism is unknown so far.
This way, innate immune signalling pathways are triggered and the secretion of several factors that regulate inflammatory response allows the expression of proinflammatory cytokines and chemokines [ 52, 53].
High expression of TREM-2 in mouse microglial cells correlate with their ability to phagocytose apoptotic neurons, hence TREM-2 might be positively regulating phagocytosis but negatively regulating inflammatory responses [36].
Evidence has shown that extracellular signal-regulated kinase (ERK) plays a decisive role in regulating inflammatory responses and neuropathic pain [ 22, 23].
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