Activation of Kupffer cells inhibits tumor growth in a murine model system

Chen, George G.; Lau, Wan Yee; Lai, Paul B.S.; Chun, Ying S.; Chak, Ernest C.W.; Leung, Billy C.S.; Lam, Isa K.Y.; Lee, Janet F. Y.; Chui, A.K.K

doi:10.1002/ijc.10412

Cited by 25 publications

(10 citation statements)

References 33 publications

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“…He clarified that Kuppfer cells produced cytotoxic factors; NO, TNF and IFN. They inhibited the tumor growth through cellular DNA damage and induced apoptosis through down regulation of Bcl-2 and upregulation of caspase-8 (Chen et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Effect of Balanites aegyptiaca on Ehrlich Ascitic carcinoma growth and metastasis in Swiss mice

Issa

Mansour

El-Safti

et al. 2015

Experimental and Toxicologic Pathology

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Section: Discussionmentioning

confidence: 99%

Effect of Balanites aegyptiaca on Ehrlich Ascitic carcinoma growth and metastasis in Swiss mice

Issa

Mansour

El-Safti

et al. 2015

Experimental and Toxicologic Pathology

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“…Both cytokines increase the FccR balance in favour of activating FccR, and are associated with a strong capacity of monocytes to respond to IgG-triggered tumour necrosis factor a production. 28 Although IFNc is produced by macrophages, 29 no up regulation of IFNc mRNA was found in the synovial layer after intra-articular injection of PLL lysozyme. By contrast, IL10 mRNA and protein levels became up regulated in wild-type synovia and seemed significantly lower in TLR42/2.…”

Section: Discussionmentioning

confidence: 99%

Toll-like receptor 4 induced FcγR expression potentiates early onset of joint inflammation and cartilage destruction during immune complex arthritis: Toll-like receptor 4 largely regulates FcγR expression by interleukin 10

Lent¹,

Blom

Grevers

et al. 2007

Annals of the Rheumatic Diseases

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Objective: To study the role of Toll-like receptor (TLR)2 and 4 in the onset of joint inflammation and cartilage destruction during immune complex-mediated arthritis (ICA), and its relationship with FccR expression. Materials and methods: ICA was induced in knee joints of TLR22/2 and TLR42/2 mice and their wild-type controls. Joint inflammation and cartilage destruction were measured in the knee joint using histology. mRNA levels were determined in synovial specimens and macrophages using quantitative polymerase chain reaction and cytokine protein levels in synovial washouts using Bioplex. Results: Joint inflammation and cartilage destruction were not different in arthritic TLR22/2 and wild-type mice. By contrast, at day 1 after ICA induction, joint swelling and proteoglycan depletion in knee joints of TLR42/2 mice were considerably lower (inflammation 68-79% and proteoglycan depletion 27-76%) when compared with wild-type controls. Cytokine production at this time point was markedly reduced in TLR42/2 mice (interleukin (IL)1, IL6, macrophage inflammatory chemokine (MIP)-1a and keratinocyte-derived chemokine 49%, 72%, 68% and 84%, respectively). In arthritic synovia of TLR42/2 mice, and also after injection of the antigen poly-L-lysine (PLL) lysozyme alone, mRNA levels of FccR, and the FccR regulating cytokine IL10 were considerably lower. Stimulation of peritoneal macrophages with PLL lysozyme up regulated mRNA levels of FccR and IL10, whereas neutralisation by anti-IL10 antibodies largely blocked FccR up regulation. At day 4, joint inflammation and cartilage destruction were comparable in TLR42/2 mice and wild-type controls. Conclusion: TLR4 regulates early onset of joint inflammation and cartilage destruction during ICA arthritis by up regulation of FccR expression and enhanced cytokine production. TLR4-mediated up regulation of FccR is largely mediated by IL10.

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“…In patients with NAFLD and other types of chronic liver disease, the accumulation of hepatic progenitors increases with the progression of fibrosis, such that the greatest enrichment with liver progenitors is observed in cirrhosis [67]. The influx of progenitors and their subsequent differentiation into mature cells is required to maintain normal tissue architecture; however, malignantly transformed progenitors are typically recognized as foreign and are targeted for deletion by the innate immune system [69]. Therefore, the emergence of HCC during efforts to repair chronic liver damage signifies a lapse in normal immune surveillance mechanisms.…”

Section: Pathogenesis and Progression In Late-stage Diseasementioning

confidence: 98%