Establishment of a cloned line of Lewis lung carcinoma cells adapted to cell culture

Bertram, John S.; Janík, P.

doi:10.1016/0304-3835(80)90130-5

Cited by 177 publications

(127 citation statements)

References 2 publications

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“…3i) protein levels in the supernatants of lung CD4 + T cells isolated from in vivo anti-IL-17A antibody-treated mice bearing tumours, when compared with untreated and IgG-treated mice. In addition, in a similar model of lung carcinoma, where the Lewis carcinoma cell line (LLC1) was injected 23 , targeted deletion of IL-17A led to induction of IFN-γ levels in the airways (Fig. 3j) confirming a negative regulatory role of IL-17A on IFN-γ production in this lung tumour model.…”

Section: Il-17a Antibody Induced Ifnγ Production By Cd4 + T Cells In mentioning

confidence: 57%

A role for T-bet-mediated tumour immune surveillance in anti-IL-17A treatment of lung cancer

et al. 2011

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Lung cancer is the leading cause of cancer deaths worldwide. The cytokine interleukin-17A supports tumour vascularization and growth, however, its role in lung cancer is unknown. Here we show, in the lungs of patients with lung adenocarcinoma, an increase in interleukin-17A that is inversely correlated with the expression of T-bet and correlated with the T regulatory cell transcription factor Foxp3. Local targeting of interleukin-17A in experimental lung adenocarcinoma results in a reduction in tumour load, local expansion of interferon-γ-producing CD4 + T cells and a reduction in lung CD4 + CD25 + Foxp3 + regulatory T cells. T-bet ( − / − ) mice have a significantly higher tumour load compared with wild-type mice. This is associated with the local upregulation of interleukin-23 and induction of interleukin-17A/interleukin-17R-expressing T cells infiltrating the tumour. Local anti-interleukin-17A antibody treatment partially improves the survival of T-bet ( − / − ) mice. These results suggest that local anti-interleukin-17A antibody therapy could be considered for the treatment of lung tumours.

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Section: Il-17a Antibody Induced Ifnγ Production By Cd4 + T Cells In mentioning

confidence: 57%

A role for T-bet-mediated tumour immune surveillance in anti-IL-17A treatment of lung cancer

et al. 2011

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“…To determine whether gaining macrophage-like features on cholesterol loading was a general phenomenon independent of cell type, we studied LLC cells, originally established from the lung of a C57BL͞6 mouse in which the murine primary LLC had been implanted (25), and NIH͞3T3 mouse fibroblasts. As shown in Fig.…”

Section: The Effects Of Cholesterol Loading On Llc Cells and Nih͞3t3 mentioning

confidence: 99%

Transdifferentiation of mouse aortic smooth muscle cells to a macrophage-like state after cholesterol loading

Rong

Shapiro

Trogan

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

449

414

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Mouse aortic smooth muscle cells (SMCs) were loaded for 72 h with cholesterol by using cholesterol:methyl-␤-cyclodextrin complexes, leading to Ϸ2-fold and Ϸ10-fold increases in the contents of total cholesterol and cholesteryl ester, respectively. Foam-cell formation was demonstrated by accumulation of intracellular, Oil Red O-stained lipid droplets. Immunostaining showed decreased protein levels of smooth muscle ␣-actin and ␣-tropomyosin and increased levels of macrophage markers CD68 and Mac-2 antigen. Quantitative real-time RT-PCR revealed that after cholesterol loading, the expression of SMC-related genes ␣-actin, ␣-tropomyosin, myosin heavy chain, and calponin H1 decreased (to 11.5 ؎ 0.5%, 29.3 ؎ 1.4%, 23.8 ؎ 1.4%, and 3.8 ؎ 0.5% of unloaded cells, respectively; P < 0.05 for all), whereas expression of macrophage-related genes CD68, Mac-2, and ABCA1 mRNA increased (to 709 ؎ 84%, 330 ؎ 11%, and 207 ؎ 13% of unloaded cells, respectively; P < 0.05 for all), thereby demonstrating that the protein changes were regulated at the mRNA level.

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“…Lewis lung (LL) is a pulmonary carcinoma cell line from B6 mice that expresses Fas but is resistant to FasL-mediated apoptosis and that can be transplanted to form tumors in vivo [39]. Primary mouse spleen cells and lymph node cells were prepared as described [40].…”

Section: Cells and Cell Linesmentioning

confidence: 99%

MHC-dependent desensitization of intrinsic anti-self reactivity

Jubala

Lamerato-Kozicki

Borakove

et al. 2008

Cancer Immunol Immunother

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The survival of naïve T cells is compromised in the absence of molecules encoded by the major histocompatibility complex (MHC) while antigen-experienced T cells survive. We hypothesized that survival pressures in an in vivo, MHC-deficient environment would permit enrichment of less frequent antigen-experienced autoreactive cells at the expense of the majority of antigen naïve T cells. To test this hypothesis, we generated MHC class I and class II-deficient mice in NOD and C57Bl/6 (B6) backgrounds, and examined the capacity of adoptively transferred autoimmune-prone NOD T cells, or non-autoimmune prone naïve B6 T cells, respectively, to reject transplanted wild type pancreatic islets or transplantable tumors in the MHC-deficient mice. In the MHC-deficient environment, CD4 T cells acquired self-hostile properties (islet rejection and tumor invasion) that were independent from their genetic propensity for autoreactivity, while CD8 T cells required appropriate prior exposure to antigen in order to survive and function (reject tumor) in this environment; however, disengagement of Tob1, a negative regulator of proliferation, led to a reverse phenotype with regard to persistence of CD4 and CD8 T cells in the MHC-deficient environment. Our data suggest that self-peptide/MHC interactions have dual roles to facilitate survival and restrain autoreactivity, thus acting as integral components of an intrinsic network of negative regulation that maintains tolerance.

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Establishment of a cloned line of Lewis lung carcinoma cells adapted to cell culture

Cited by 177 publications

References 2 publications

A role for T-bet-mediated tumour immune surveillance in anti-IL-17A treatment of lung cancer

A role for T-bet-mediated tumour immune surveillance in anti-IL-17A treatment of lung cancer

Transdifferentiation of mouse aortic smooth muscle cells to a macrophage-like state after cholesterol loading

MHC-dependent desensitization of intrinsic anti-self reactivity

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