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The Many Roles of Chemokines and Chemokine Receptors …
NKT cells are activated by self- or microbial-lipid antigens, or by signaling through toll-like receptors (TLR), and act as a bridge between innate and adaptive immunities. Following activation, NKT cells rapidly secrete either pro-inflammatory or anti-inflammatory cytokines and chemokines, and thereby determine the direction for subsequent immunity or tolerance.
LSEC and KCs are likely to be the first resident cells that CTCs encounter in the liver. The tumor cells can be eliminated by local, tumoricidal KCs. KCs can also activate other innate immune response cells such as NK cells, NKT cells, and neutrophils. NK cells can mediate antitumor cytotoxicity by secreting perforin/granzyme or through CD95/CD95L pathway. Cytokines and chemokines such as TNF-α, IL-8, and CXCL10 can activate resident tumoricidal macrophages, as well as recruit host immune cells with anti-tumor activities .
CCL5: A Double-Edged Sword in Host Defense Against …
Figure 3: Liver immune microenvironment and tumor growth. A: immune attack on circulating tumor cells. Circulating tumor cells entering the sinusoidal area are attacked by immune cells in the sinusoid, especially Kupffer cells and NK cells. These cells eliminate tumor cells via phagocytosis, cytotoxic granules, death-receptor pathways, nitric oxide, or ROS; B: extravasation of tumor cells into the hepatic parenchyma. Following firm attachment to LSEC via adhesion molecules such as E-selection, VCAM-1, and ICAM-1, tumor cells escape from the sinusoidal space and invade into the extrasinusoidal space, which is rich in various growth factors such as HGF and IGF-1; C: remodeling of hepatic parenchyma and angiogenic sprouting. Tumor cell invasion into the extrasinusoidal space triggers HSC and M2 macrophage recruitment into the tumors and increases production of collagen in and around hepatic metastases. HSC recruited into the metastases as myofibroblasts release growth factors, cytokines, and MMPs. IL-8 produced by HSC induces the expression of VEGFR2 and VEGF on endothelial cells and mediates autocrine and paracrine stimulation of vascular endothelium; D: rapid growth of hepatic metastasis. Vascular endothelial cells are further recruited to the tumor site and tumors become further vascularized. The vascularization of tumor results in rapid growth of metastasis. Local production of Th-2 type cytokines, deprivation of tryptophan, and elimination of activated T cells via PD-L/PD-L1 interaction result in non-T cell inflamed immune microenvironment in the hepatic metastasis. CXCR9: chemokine (C-X-C motif) ligand 9; CXCR10: chemokine (C-X-C motif) ligand 10; CCR5: C-C chemokine receptor 5; Fas L: fas ligand; HSC: hepatic stellate cell; HGF: hepatocyte growth factor; IL-6: interleukin 6; IL-8: interleukin 8; IL-10: interleukin 10; IFN-g: interferon gamma; IGF-1: insulin growth factor-1; KC: kupffer cell; LSEC: liver sinusoidal endothelial cell; NO: nitric oxide; PD 1: programmed death 1; PD-L1: programmed death ligand 1; TDO: tryptophan 2,3 dioxtgenase; TGF-b: transforming growth factor beta; T reg: regulatory t Cell; VCAM-1: vascular cell adhesion protein 1; VEGF: vascular endothelial growth factor; VLA-4: very late antigen 4; ROS: reactive oxygen species
The Many Roles of Chemokines and Chemokine …
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