Immortalization of macrophages from mouse bone marrow and fetal liver

Gandino, Lucia; Varesio, Luigi

doi:10.1016/0014-4827(90)90159-8

Cited by 17 publications

(14 citation statements)

References 21 publications

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“…Heat inactivation was achieved by incubating the bacteria at 80°C for 30 minutes. Immortalized macrophage cell lines from wild type, rip2−/− , nod2−/− and nod1−/−nod2−/− mice were established by infecting bone marrow cells with a v-raf/mil and v-myc retrovirus in the presence of GM-CSF and polybrene [75],[76]. These rip2−/− , nod2−/− and nod1−/−nod2−/− macrophage cell lines express CD11b and Gr-1 and are capable of phagocytosing antibody coated beads.…”

Section: Methodsmentioning

confidence: 99%

NOD2, RIP2 and IRF5 Play a Critical Role in the Type I Interferon Response to Mycobacterium tuberculosis

et al. 2009

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While the recognition of microbial infection often occurs at the cell surface via Toll-like receptors, the cytosol of the cell is also under surveillance for microbial products that breach the cell membrane. An important outcome of cytosolic recognition is the induction of IFNα and IFNβ, which are critical mediators of immunity against both bacteria and viruses. Like many intracellular pathogens, a significant fraction of the transcriptional response to Mycobacterium tuberculosis infection depends on these type I interferons, but the recognition pathways responsible remain elusive. In this work, we demonstrate that intraphagosomal M. tuberculosis stimulates the cytosolic Nod2 pathway that responds to bacterial peptidoglycan, and this event requires membrane damage that is actively inflicted by the bacterium. Unexpectedly, this recognition triggers the expression of type I interferons in a Tbk1- and Irf5-dependent manner. This response is only partially impaired by the loss of Irf3 and therefore, differs fundamentally from those stimulated by bacterial DNA, which depend entirely on this transcription factor. This difference appears to result from the unusual peptidoglycan produced by mycobacteria, which we show is a uniquely potent agonist of the Nod2/Rip2/Irf5 pathway. Thus, the Nod2 system is specialized to recognize bacteria that actively perturb host membranes and is remarkably sensitive to mycobacteria, perhaps reflecting the strong evolutionary pressure exerted by these pathogens on the mammalian immune system.

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Section: Methodsmentioning

confidence: 99%

NOD2, RIP2 and IRF5 Play a Critical Role in the Type I Interferon Response to Mycobacterium tuberculosis

et al. 2009

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“…In addition, Franz et al [25] have described the establishment of macrophage cell lines from mouse bone marrow and spleen using a retrovirus, AF-1. More recently the recombinant J2 virus carrying two known oncogenes, v-myc and v-raf/mil, has been used to generate macrophage lines from mouse bone marrow and fetal liver [7,8]. Two macrophage cell lines derived from AKR mouse bone marrow carry the AKR murine leukaemia virus [26].…”

Section: Discussionmentioning

confidence: 99%

“…Transformation by SV-40 virus can give rise to monocyte/macrophage cell lines [4] and transfection with defective SV-40 DNA has also been used [5,6]. More recently mouse macrophage cell lines have been generated by infection with oncogene-carrying retroviruses [7,8].…”

Section: Introductionmentioning

confidence: 99%

The characteristics of macrophage-like cell lines derived from normal sheep spleens

Ögmundsdóttir

Hardarson

Steinarsdóttir³

et al. 1991

FEMS Microbiology Letters

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Macrophage‐like cell lines were derived from sheep spleens using conditioned medium from L‐929 mouse cells as a source of colony stimulating factor. In seven out of ten attempts colonies of macrophage‐like cells appeared after 2–3 weeks of culture. The cells were established in culture as cell lines, and survived 120 passages. They were strongly (++) positive for non‐specific esterase but negative for peroxidase and produced detectable but small amounts of lysozyme (0.21–1.76 μg/106 cells). Latex particles were actively phagocytosed. Bacteria (Staphylococcus albus, Staphylococcus aureus) attached to the cell surface and were internalized in the presence of specific antibody. Expression of receptors for immunoglobulin and complement varied somewhat between the different cell lines; the proportion of receptor‐bearing cells ranged between 9 and 26% FC‐receptors, and 10 and 38% for C‐receptors. The cell lines displayed a peculiar karyotype as well as protein profile that were different from normal sheep but similar between the different cell lines. Culture supernatants of the cell lines contained a colony stimulating activity which was used to establish further cell lines. They also spontaneously produced an interleukin‐1‐like activity that had no effect on baseline proliferation of sheep lymphocytes but enhanced their response to PHA (1.7‐fold) particularly in conjunction with sheep IL‐2 (4‐fold). Prostaglandin E2 was produced in a growth‐cycle dependent manner: the peak production occured on the second day (77–140 pg/ml) at 2 × 105 cells and declined to 33–50 pg/ml on the eighth day when cell numbers had increased to 2–3 × 10106. These easily cultured cell lines derived from normal tissue without the introduction of viral DNA should provide a useful source of material for studies of macrophage function in sheep.

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“…Experiments using HUVEC were carried out after a maximum of six passages. Murine BMDMs immortalized using J2 viurs (iBMDM) (Gandino and Varesio, 1990) were a gift of Andrea Oeckinghaus and grown in DMEM medium supplemented with 10% FCS and conditioned medium (10–30% L929 cell supernatant).…”

Section: Methodsmentioning

confidence: 99%

YOD1/TRAF6 association balances p62-dependent IL-1 signaling to NF-κB

Schimmack

Schorpp

Kutzner

et al. 2017

eLife

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The ubiquitin ligase TRAF6 is a key regulator of canonical IκB kinase (IKK)/NF-κB signaling in response to interleukin-1 (IL-1) stimulation. Here, we identified the deubiquitinating enzyme YOD1 (OTUD2) as a novel interactor of TRAF6 in human cells. YOD1 binds to the C-terminal TRAF homology domain of TRAF6 that also serves as the interaction surface for the adaptor p62/Sequestosome-1, which is required for IL-1 signaling to NF-κB. We show that YOD1 competes with p62 for TRAF6 association and abolishes the sequestration of TRAF6 to cytosolic p62 aggregates by a non-catalytic mechanism. YOD1 associates with TRAF6 in unstimulated cells but is released upon IL-1β stimulation, thereby facilitating TRAF6 auto-ubiquitination as well as NEMO/IKKγ substrate ubiquitination. Further, IL-1 triggered IKK/NF-κB signaling and induction of target genes is decreased by YOD1 overexpression and augmented after YOD1 depletion. Hence, our data define that YOD1 antagonizes TRAF6/p62-dependent IL-1 signaling to NF-κB.DOI: http://dx.doi.org/10.7554/eLife.22416.001

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Immortalization of macrophages from mouse bone marrow and fetal liver

Cited by 17 publications

References 21 publications

NOD2, RIP2 and IRF5 Play a Critical Role in the Type I Interferon Response to Mycobacterium tuberculosis

NOD2, RIP2 and IRF5 Play a Critical Role in the Type I Interferon Response to Mycobacterium tuberculosis

The characteristics of macrophage-like cell lines derived from normal sheep spleens

YOD1/TRAF6 association balances p62-dependent IL-1 signaling to NF-κB

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