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. 2015 Jan 2;179(2):161–172. doi: 10.1111/cei.12476

Figure 2.

Figure 2

Mechanisms illustrated are selected experimentally supported concepts. (1) Inhibition of serine-proteases interferes with activation of immune-related protease-activated receptors (PARs); (2) direct binding to interleukin (IL)-8 interferes with neutrophil recruitment; (3) inhibition of ADAM metallopeptidase domain 17 (ADAM17) interferes with release of tumour necrosis factor (TNF)-α; (4) binding to TNF receptors (TNFR) at high concentrations interferes with TNF-α-induced pathways; (5) up-regulation of IL-10 release by multiple cell types exerts an anti-inflammatory environment, and joins α1-anti-trypsin (AAT) in (6) up-regulation of IL-1Ra, which will interfere with the IL-1 pathway. (7) Release of pro-IL-1β from necrotic cells results in active IL-1β upon engagement with serine-proteases, the targets of AAT. (8) Necrotic cells contribute potent adjuvants to the immune system; gp96 chaperones antigens and then binds to CD91, which promotes their processing and loading on major histocompatibility complex (MHC) class I 42. AAT was shown to both (8) bind to gp96, thus neutralizing its inflammatory activity 40, and to (9) CD91 43.