1. Figure 4 Macrophages in liver inflammation
Figure 4 | Macrophages in liver inflammation. Inflammatory macrophages largely derive from infiltrating monocytes recruited from blood and bone marrow via chemokines such as CCL2 or CCL1 in response to danger and TLR signals. Dependent on their stage of activation they perform various inflammatory functions including secretion of inflammatory cytokines like TNF, IL-1β and IL-18, associated with the M1 macrophage phenotype, as well as pro-fibrogenic mechanisms such as HSC activation. Macrophages can also exhibit restorative functions (classically associated with the M2 and MREG macrophage phenotypes) such as suppressing inflammation and extracellular matrix reorganisation by the secretion of matrix degrading enzymes. They also perform intensive crosstalk with passenger lymphocytes, skewing for example, T cells into pro-inflammatory TH1, alternative TH2 or anti-inflammatory TREG responses. ALD, alcoholic liver disease; Arg-1, Arginase-1; CLD, chronic liver disease; Col-1, collagen type I; DC, dendritic cell; HMGB1, high mobility group box protein 1; IDO, indolamine 2,3-dioxigenase; iNOS, induced nitric oxide synthase; IRF3, interferon regulatory factor 3; LPS, lipopolysaccharide; LSEC, liver sinusoidal endothelial cell; M-CSF, macrophage colony stimulating factor; MMP, matrix metalloproteinase; MoMF, monocyte-derived macrophage; MYD88, myeloid differentiation primary response gene 88; NK cell, natural killer cell; PD-L1, programmed death ligand 1; PGE2, prostaglandin E2; PI3K, phosphoinositol 3-kinase; TGFβ, transforming growth factor β; TIMP, tissue inhibitor of metalloproteinases; TLR, Toll-like receptor; TRIF, TIR-domain-containing adaptor-inducing interferon-beta; VEGF, vascular endothelial growth factor.
Heymann, F. & Tacke, F. (2016) Immunology in the liver — from homeostasis to disease
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro