Female c57bl 6 wt mice

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Female C57BL/6 (WT) mice are laboratory animals commonly used in biomedical research. They are genetically unmodified and serve as a standard control group for various studies.

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C57bl 6 mice, by Charles River Laboratories (1 mentions) Rag1 mice, by Jackson ImmunoResearch (1 mentions)

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C57BL/6 mice (4025 citations) C57BL/6 (2462 citations) WT C57BL/6 mice (265 citations) C57BL/6 WT (133 citations) WT mice (39 citations) C57BL/6 females (30 citations) Female WT mice (2 citations)

8 protocols using female c57bl 6 wt mice

Generation and Utilization of IL-21R-/- Mice

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The B16F0 mouse melanoma cell line was kindly provided by Dr. J. Galipeau (Atlanta, GA, USA). The RAG2p‐GFP transgenic mice were kindly provided by Dr. M. Nussenzweig (Rockefeller University, New York, NY, USA). Female WT C57BL/6 mice were purchased from the Jackson Laboratory (Bar Harbor, ME, USA). To generate IL‐21R^−/− C57BL/6 mice, commercially available sperm was purchased from the MMRRC repository and used to fertilize Female WT C57BL/6 mice. All mice were housed at the Institute for Research in Immunology and Cancer (IRIC) animal facility under specific pathogen‐free conditions. All animal protocols were approved by the Animal Care Committee of Université de Montréal.

Al‐Chami E., Tormo A., Pasquin S., Kanjarawi R., Ziouani S, & Rafei M. (2016). Interleukin‐21 administration to aged mice rejuvenates their peripheral T‐cell pool by triggering de novo thymopoiesis. Aging Cell, 15(2), 349-360.

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Generation and Validation of Transgenic Mice

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Female WT C57BL/6 mice were purchased from Jackson Laboratory (Catalog #000664, Bar Harbor, Maine). The generation of H-2K^b LoxP parental mice and the MHC class I deficient CMV-Cre parental mice are detailed in our previous work(24 (link)). Genotypes were confirmed by PCR for Cre-Recombinase using primers from the Jackson Laboratory. Flow cytometry for surface H-2K^b MHC class I surface protein ensured the appropriate identity of all experimental animals. Mice were bred and maintained in the animal facility at Mayo Clinic under IACUC guidelines. Animal handling and all procedures were done in the manner approved by the Mayo Clinic Institutional Animal Care and Use Committee.

Yadava A., Kumar S., Dvorak J.A., Milon G, & Miller L.H. (1996). Trafficking of Plasmodium chabaudi adami-infected erythrocytes within the mouse spleen.. Proceedings of the National Academy of Sciences of the United States of America, 93(10), 4595-4599.

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APCMin/+ Mouse Model for Colorectal Cancer

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All animal experiments described herein were approved by the Stanford University Institutional Animal Care and Use Committee. Breeding pairs of APC^Min/+ male and WT C57BL/6 female mice were purchased from The Jackson Laboratory and bred on-site. OT-II TCR transgenic Rag^−/− mice were purchased from Taconic. All mice were housed in an American Association for the Accreditation of Laboratory Animal Care accredited animal facility, and maintained in pathogen-free conditions on standard rodent chow ad libitum unless otherwise stated.

Penny H.L., Prestwood T.R., Bhattacharya N., Sun F., Kenkel J.A., Davidson M.G., Shen L., Zuniga L.A., Seeley E.S., Pai R., Choi O., Tolentino L., Wang J., Napoli J.L, & Engleman E.G. (2016). Restoring Retinoic Acid Attenuates Intestinal Inflammation and Tumorigenesis in APCMin/+ Mice. Cancer immunology research, 4(11), 917-926.

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Isolation and Use of Murine Immune Cells

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For isolation of naïve AMs, 6–8-wk-old WT C57Bl/6 female mice (Jackson Laboratory) were used. For CS experiments, 6–8-wk-old mice harboring a targeted deletion of both alleles of the Ptger2 gene encoding the EP2 receptor (EP2 KO) were used. These mice were originally provided by Dr. Richard Breyer (Vanderbilt University) (Kennedy et al, 1999 (link)) and were maintained/bred by the University of Michigan Unit of Laboratory Medicine. For aging experiments, 8-wk-old (young) and 18–22-mo-old (aged) female C57Bl/6 mice were procured from Charles River or the National Institute of Aging Animal Facility, respectively. All mice were maintained at the University of Michigan Unit for Laboratory Animal Medicine. Animals were treated according to National Institutes of Health guidelines for the use of experimental animals with the approval of the University of Michigan Committee for the Use and Care of Animals.

Penke L.R., Speth J.M., Draijer C., Zaslona Z., Chen J., Mancuso P., Freeman C.M., Curtis J.L., Goldstein D.R, & Peters-Golden M. (2020). PGE2 accounts for bidirectional changes in alveolar macrophage self-renewal with aging and smoking. Life Science Alliance, 3(11), e202000800.

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Alcoholic Liver Disease Mouse Model

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Female C57/BL6 (WT) mice aged 12 wk were obtained from Jackson Laboratory. Mice genetically deficient for Cx32 (Cx32KO) were obtained from K. Willecke (University of Bonn) and D. Paul (Harvard University). IRF3 KO mice were generated by Tadatsugu Taniguchi and obtained from E. Rosen (Harvard University). Hepatocyte-specific cGAS KO mice were generated with the Cre-Lox system. Mice expressing a floxed cGas exon 2 (cGAS F/F) were backcrossed to C57BL/6J mice (30 (link)). These mice were obtained from C. Rice (Rockefeller University). The mice were then crossed with albumin-Cre mice to create mice with cGAS deficiency only in hepatocytes (cGAS LKO). STING KO mice were obtained from H. Reinecker (Harvard University). To induce alcoholic hepatitis, we followed the protocol outlined in the National Institute on Alcohol Abuse and Alcoholism (NIAAA) chronic and binge model (31 (link)). To induce chronic alcohol-related liver disease, we used the classic Lieber-DeCarli model for 6 wk (21 (link)). Alcohol and PF diets were obtained from BioServ. To determine whether Cx32 deficiency offers survival benefit against ethanol-induced liver injury, we placed Cx32KO and WT mice, which were treated with 2APB at a dose of 20 mg/kg administered daily by intraperitoneal injection, on a 6% ethanol-containing liquid diet (32 ).

Luther J., Khan S., Gala M.K., Kedrin D., Sridharan G., Goodman R.P., Garber J.J., Masia R., Diagacomo E., Adams D., King K.R., Piaker S., Reinecker H.C., Yarmush M.L., Argemi J., Bataller R., Dienstag J.L., Chung R.T, & Patel S.J. (2020). Hepatic gap junctions amplify alcohol liver injury by propagating cGAS-mediated IRF3 activation. Proceedings of the National Academy of Sciences of the United States of America, 117(21), 11667-11673.

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Murine Model Generation and Maintenance

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Female C57BL/6 (WT) mice were purchased from the Jackson Laboratory (Bar Harbor, ME). Cbl-b^−/− mice on a C57BL/6 background were a gift from Dr. H. Gu (Columbia University, New York, NY). RAG-1^−/− mice were purchased from the Jackson Laboratory and bred and maintained in our facility. All mice were maintained and bred under specific pathogen-free conditions in accordance with the guidelines of the Center for Laboratory Animal Care at the University of Connecticut Health Center (Farmington, CT).

Fujiwara M., Anstadt E.J., Khanna K.M, & Clark R.B. (2015). Cbl-b-Deficient Mice Express Alterations in Trafficking-Related Molecules but Retain Sensitivity to the Multiple Sclerosis Therapeutic Agent, FTY720. Clinical immunology (Orlando, Fla.), 158(1), 103-113.

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Congenic C57BL/6 Mouse Models

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Female C57BL/6 (WT) mice were purchased from the Jackson Laboratory (Bar Harbor, ME, USA). Cbl-b^−/− mice on a C57BL/6 background were a gift from Dr. H. Gu (Columbia University, New York, NY, USA). Female C57BL/6 congenic mice (CD45.1⁺) were also purchased from the Jackson Laboratory. All mice were maintained and bred under specific pathogen-free conditions in accordance with the guidelines of the UConn Health Institutional Animal Care and Use Committee (IACUC) and the Center for Comparative Medicine at UConn Health. The UConn Health IACUC has approved the protocol (protocol 101448-0919) used in these studies.

Fujiwara M., Anstadt E.J, & Clark R.B. (2017). Cbl-b Deficiency Mediates Resistance to Programmed Death-Ligand 1/Programmed Death-1 Regulation. Frontiers in Immunology, 8, 42.

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Osteoblast Differentiation and Mineralization

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Female C57BL/6 (WT) mice were purchased from Jackson Labs (Bar Harbor, ME). Toll-like receptor knockout (TLR2−/−) mice, bred onto a C57BL/6 background, were a generous gift of Dr. S. Akira (Osaka University, Japan) (15 (link)). All mice were bred in accordance with University of Connecticut Center for Laboratory Animal Care regulations. Mouse calvaria harvested from 5–7 day old wild-type and TLR2−/− mice were digested with collagenase and trypsin. Calvarial osteoblasts were plated at a cell density of 1.5 × 10⁴/cm². For the first week, the cells were differentiated in Dulbecco’s minimal essential medium (DMEM). Differentiation in the second and third weeks took place in α-MEM that contained ascorbic acid and β-glycerol phosphate. Treatment groups were divided into vehicle control, 1.2 µg/ml of P. endodontalis total lipid extract and 1.2 µg/ml of P. gingivalis total lipid extract in the form of sonicated liposomes (3 watts for 90 seconds). Lipids were added to osteoblast cultures at 3 day intervals for the second and third weeks of culture based on the previous characterization of P. gingivalis lipid effects on osteoblasts (16 (link)). At 21 days, the culture medium was removed and osteoblast differentiation was evaluated by staining for alkaline phosphatase production as well as von Kossa staining for mineral deposition (16 (link)).

Mirucki C.S., Abedi M., Jiang J., Zhu Q., Wang Y.H., Safavi K.E., Clark R.B, & Nichols F.C. (2014). Biologic Activity of Porphyromonas endodontalis complex lipids. Journal of endodontics, 40(9), 1342-1348.

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