MiRNA-29b can target the PI3K/AKT pathway to prevent liver fibrosis by attenuating HSC activation and inducing apoptosis[88]. many pathways involved need to be further studied. This review mainly focuses on the crosstalk regulatory network among inflammatory cells, cytokines, and the related signaling pathways in the pathogenesis of chronic inflammatory liver diseases. Moreover, we also summarize the recent studies on the mechanisms underlying liver fibrosis and clinical efforts on the targeted therapies against the fibrotic CD36 response. the HLA-G-mediated decrease of collagen I, and IL-10 also mediates crosstalk between mast cells and HSCs[8]. Endothelial progenitor cells dramatically inhibit the proliferation, adhesion, and migration of HSCs, promote the apoptosis of HSCs, and down-regulate the mRNA and protein expression of collagen I and collagen III in HSCs[9]. Epigenetic crosstalk between histone acetylation and miRNAs inhibited HSC activation[10]. Researchers have explored drugs targeting HSCs. A number of protein markers were found to be overexpressed in activated HSCs, and their ligands have been utilized to specifically deliver various anti-fibrotic agents[11]. Natural killer (NK) cells are important in regulating hepatic fibrosis, and their cytotoxic killing of HSCs has been reported. Activated NK cells lead HSCs to death in a TRAIL-involved mechanism the p38/PI3K/AKT pathway, which suggested that the p38/PI3K/AKT pathway in NK cells may be a novel drug target to inhibit liver fibrosis[12]. It has been confirmed that activation of HSCs could be inhibited by reducing the production of transforming growth factor-1 (TGF-1) in HSCs inhibition of the NF-B pathway through downregulation of the TGF-1/Smad3 pathway[13]. Kupffer cells Kupffer cells as resident macrophages are one of important liver inflammatory cell types, and account for 30% of sinusoidal cells[14]. Activated Kupffer cells secrete abundant cytokines and signaling molecules, which enhance liver immunopathology. Activated Kupffer cells participate in the initial injury/fibrogenic response to TGF-1 and methotrexate, which results in upregulated production of cytokines, including IL-10, IL-4, IL-6, and IL-13[15]. CXCL6 stimulates the phosphorylation of epidermal growth factor receptor (EGFR) and the expression of TGF- in cultured Kupffer cells, thereby resulting in activation of HSCs[16]. In response to liver injury induced by endotoxin, IL-35 can promote Kupffer cells to secrete IL-10 and reduce acute liver injury[17]. A crosstalk network AM 2201 including Ly6C+ AM 2201 monocytes, CCL2-CCR2, and Kupffer cells determines HBV clearance/tolerance, and manipulation of these two cell types may be a potential strategy for immunotherapy of HBV-related liver diseases[18]. Activation of Kupffer cells by pathogens and the CCL2/CCR2 axis can be the key factor to recruit innate effector cells to the injured liver[19]. In alcoholic liver disease mice, a crosstalk network including Kupffer cells, T cells, CCL2/CCR2, and CCL5/CCR5 sensitizes hepatocytes[20]. NLRP3 inflammasome from Kupffer cells is involved in the occurrence of schistosomiasis-induced liver fibrosis (SSLF) NF-B signaling and IL-1 in serum increased strongly[21]. An effective method of isolating Kupffer cells was explored to eliminate endothelial cell contamination, which could be meaningful for illuminating Kupffer cell function and mechanism in diseases[22]. RAMP 1 in Kupffer cells mediates a AM 2201 crosstalk network involving infiltration of immune cells and pro-inflammatory cytokines secreted by Kupffer cells and splenic T cells, and such crosstalk network can regulate the immune response[23]. ATG5-dependent autophagy involved in crosstalk between Kupffer cells and cytokines (IL-6 and IL-10) mediated acute liver injury response[24]. The cross communication of Sphk1 with HSCs and Kupffer cells regulated the CCL2-CCR2 axis in liver fibrosis[25]. Fas ligand stimulated Fas-expressing Kupffer cells or macrophages to secrete active IL-18 in a caspase-1-independent manner and finally resulted in acute liver injury in mice[26]. Kupffer cells with high expression of CD1d only presented lipid antigen to NKT cells for activation of the pro-inflammatory cytokine pathway[27]. Huangqi decoction activated Kupffer cells.