2d2 mice

Manufactured by Jackson ImmunoResearch

Sourced in United States

2D2 mice are a type of laboratory mouse model developed by Jackson ImmunoResearch. They are genetically modified to express a specific receptor on the surface of their T cells, which is useful for research purposes. The core function of 2D2 mice is to serve as a tool for immunological and neurological studies.

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Lab products found in correlation

C57bl 6 mice, by Jackson ImmunoResearch (4 mentions) C57bl 6, by Taconic Biosciences (1 mentions) C57bl 6, by Jackson ImmunoResearch (1 mentions) γhv68 wums strain, by American Type Culture Collection (1 mentions)

Spelling variants of this product

2D2 TCR transgenic mice (16 citations) 2D2 TCR transgenic (2D2 Tg) mice (2 citations) MOG 35–55 specific TCR transgenic/ 2D2 mice (2 citations) C57BL/6 and 2D2 mice (2 citations)

8 protocols using 2d2 mice

Genetically Engineered Mouse Models for Immunology

Cited 4 times

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Gata3^fl/fl [Taconic line 355 (36 (link))], Cre-ERT2-Gata3^fl/fl mice [Taconic line 8445 (37 (link))], Cd45.1/Cd45.2 C57BL/6 (Taconic line 8422), Cd45.1 C57BL/6 (Taconic line 7), Tcra^-/- (Taconic line 98) and C57BL/6 mice were ordered from the NIAID-Taconic repository or the Taconic. hCd2^CreGata3^fl/fl mice has been reported recently (38 (link)). Tbx21^Cre mice [Jax line 024507 (39 (link))] were crossed with Gata3^fl/fl mice to generate Tbx21^CreGata3^fl/fl mice. Rorc^E2-Crimson mice (35 (link)) were crossed with Gata3^ZsGreen (40 (link)) and Foxp3^RFP [Jax line 008374 (41 (link))] reporter mice to generate Rorc^E2CrimsonGata3^ZsGreenFoxp3^RFP triple reporter mice. 2D2 mice were purchased from the Jackson Laboratory (JAX line 006912). All mice were imported, bred, and housed within the National Institute of Allergy and Infectious Diseases (NIAID) specific pathogen-free animal facilities. Unless otherwise specified, all experimental mice were used between 6-16 weeks of age under an animal study protocol approved by the NIAID Animal Care and Use Committee.

Butcher M.J., Gurram R.K., Zhu X., Chen X., Hu G., Lazarevic V., Zhao K, & Zhu J. (2023). GATA3 induces the pathogenicity of Th17 cells via regulating GM-CSF expression. Frontiers in Immunology, 14, 1186580.

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Mouse Models for Immunological Studies

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Eight to 12 weeks old C57BL/6 mice and 2D2 mice (C57BL/6 background) were purchased from the Jackson Laboratory (Bar Harbor, ME, USA). Dr. J.-C. Renauld (Ludwig Institute, Brussels, Belgium) and Dr. A.N.J McKenzie (MRC Laboratory of Molecular Biology, Cambridge, UK) kindly provided homozygous breeding pairs of IL-9R^−/− and IL-9^−/− mice on the C57BL/6 background. For all experiments, age and sex-matched mice were used. Every effort was made to minimize the suffering of mice. Thomas Jefferson University’s Institutional Animal Care and Use Committee approved all experiments described in this study.

Yoshimura S., Thome R., Konno S., Mari E.R., Rasouli J., Hwang D., Boehm A., Li Y., Zhang G.X., Ciric B, & Rostami A. (2019). IL-9 controls CNS autoimmunity by suppressing GM-CSF production. Journal of immunology (Baltimore, Md. : 1950), 204(3), 531-539.

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Mouse Strain Acquisition and Approval

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Eight- to 12-week old wild-type (WT) female C57BL/6 mice were obtained from Jackson Laboratory (Bar Harbor, ME). Lgals1^−/− mice on C57BL/6 background were kindly provided by Dr. José Conejo-Garcia (Wistar Institute, Philadelphia, PA) and Dr. Naveen Rajasagi (University of Tennessee, Knoxville, TN). These mice were previously described by Poirier and Robertson [46 (link)]. 2D2 mice on C57BL/6 background were purchased from Jackson Laboratory (Bar Harbor, ME). Experimental protocols were approved by the Institutional Animal Care and Use Committee of Thomas Jefferson University.

Mari E.R., Rasouli J., Ciric B., Moore J.N., Conejo-Garcia J.R., Rajasagi N., Zhang G.X., Rabinovich G.A, & Rostami A. (2016). Galectin-1 is essential to intravenous tolerance induction in experimental autoimmune encephalomyelitis. European journal of immunology, 46(7), 1783-1796.

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Transgenic Mouse Model Characterization

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2D2 mice were obtained from Jackson Laboratories (Bar Harbor, ME, USA), and wild-type C57BL/6 mice were obtained from the Animal Research Center of Shanxi Medical University. All procedures in the present study were approved by the Shanxi Committee on Ethics of Animal Research. All mice in these studies were group-housed at 22~24°C and were fed and watered ad libitum. The male and female 2D2 transgenic mice were mated with C57BL/6 wild-type mice (1: 1). Genomic DNA was isolated from the tails of baby mice and analyzed using PCR, as previously described [15 ].
Two groups of mice were used: the experimental group, consisting of the positive baby mice from 2D2 transgenic mice (n=24); and control group, consisting of the C57BL/6 mice (n=24).

Xue H., Cao X, & Zhang M. (2018). Alteration of Circadian Rhythms in 2D2 Transgenic Mice. Medical Science Monitor : International Medical Journal of Experimental and Clinical Research, 24, 8272-8278.

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Inducing EAE in γHV-68 Infected Mice

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C57Bl/6 mice, C57Bl/6 CD40KO mice and 2D2 mice were purchased from the Jackson Laboratory and were bred and maintained in our rodent facility at the University of British Columbia. Mice were infected intraperitoneally (i.p.) between 7–10 weeks of age with 10⁴ pfu of γHV-68 WUMS strain (purchased from ATCC, propagated on BHK cells); or 10⁴ pfu of latency deficient γHV-68 AC-RTA (originally developed by Dr. Ting-Ting Wu, generous gift of Dr. Marcia A. Blackman)36 (link); or 200 μl of MEM as a control. EAE was induced 35–40 days post infection by injecting subcutaneously each mouse with 100μl of emulsified complete Freund’s adjuvant (DIFCO) with 200μg of MOG 35-55 (GenWay biotech, purity >95%) and 400 μg of desiccated Mycobacterium tuberculosis H37ra (DIFCO). Mice also received two i.p. injections with 200 ng of pertussis toxin (List Biologicals) at time of immunization and 48 hours later. Mice were scored on a scale of 0 to 5: 0, no clinical signs; 0.5, partially limp tail; 1, paralyzed tail; 2 loss of coordinated movements; 2.5; one hind limb paralyzed; 3, both hinds limbs paralyzed; 3.5, hind limbs paralyzed, weakness in the forelimbs; 4, forelimbs paralyzed; 5, moribund or dead

Casiraghi C., Citlali Márquez A., Shanina I, & Steven Horwitz M. (2015). Latent virus infection upregulates CD40 expression facilitating enhanced autoimmunity in a model of multiple sclerosis. Scientific Reports, 5, 13995.

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Genetic Modeling of Autoimmune Disorders

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Animal protocols were approved by the Washington University Animal Studies Committee. MiR-223^−/− and littermate-derived wild-type (WT) mice (C57Bl/6 background) were obtained from Dr. Todd Fehniger and bred at Washington University. The miR-223 gene is located on the X chromosome, and mice were bred as miR-223^−/y or littermate miR-223^+/y (termed WT throughout the manuscript) males with heterozygous females. MiR-223^−/− and WT mice deriving from these breeding pairs were used in all experiments. C57BL/6 mice transgenic for a TCR with specificity for the peptide MOG_35–55 (TCR^MOG mice, also referred to as 2D2 mice; The Jackson Laboratory) were screened by flow cytometric analysis of peripheral blood cells using a specific antibody to Vβ11 (BD Biosciences) [3 (link)]. Mice were 6–9 weeks of age at the initiation of the studies.

Cantoni C., Cignarella F., Ghezzi L., Mikesell B., Bollman B., Berrien-Elliott M.M., Ireland A.R., Fehniger T.A., Wu G.F, & Piccio L. (2016). Mir-223 regulates the number and function of myeloid-derived suppressor cells in multiple sclerosis and experimental autoimmune encephalomyelitis. Acta neuropathologica, 133(1), 61-77.

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Murine Model of Autoimmune Neuroinflammation

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Female C57BL/6 mice 6–7 wk of age were purchased from the National Cancer Institute; females were used for all experiments. 2D2 mice (T cell receptor specific for MOG on a C57BL/6 background) were purchased from The Jackson Laboratory and bred in house. All studies were approved by the Johns Hopkins University School of Medicine Animal Care and Use Committee.

Glenn J.D., Smith M.D., Xue P., Chan-Li Y., Collins S., Calabresi P.A., Horton M.R, & Whartenby K.A. (2017). CNS-targeted autoimmunity leads to increased influenza mortality in mice. The Journal of Experimental Medicine, 214(2), 297-307.

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Generation of Swap70-/- x 2D2 x Foxp3GFP Mice

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Foxp3^GFP mice (38 (link)) were crossed to Swap-70^-/- mice (39 (link)) to generate Swap70^-/- x Foxp3^GFP mice. Foxp3^RFP/GFP mice expressing the Cre recombinase GFP (GFP-Cre) fusion protein as a Foxp3 BAC transgene and the RFP reporter from an internal ribosome entry site (IRES) downstream of the Foxp3 coding region (Foxp3^IRES-RFP) have been previously described (40 (link)). Foxp3^GFP mice were bred to 2D2 mice (Jackson Laboratory), expressing the transgenic, self-reactive Vα3.2 (2D2) T cell receptor (TCR) specific for myelin oligodendrocyte glycoprotein [MOG, (41 (link))] to generate Foxp3^GFP x 2D2-MOG mice. Foxp3^GFP x 2D2-MOG mice were then bred with Swap70^-/- mice to obtain Swap70^-/- x 2D2 x Foxp3^GFP mice. All mice were on C57/BL6 background and were housed and bred either at the animal facility of the CRTD, TU Dresden or the Experimental Center of the Medizinisch-Theoretisches Zentrum, TU Dresden. Animal experiments were performed as approved by the Regierungspräsidium Dresden (AZ 24-9168.24-1/2014-5, 24-9168.24-1/2014-1).

Dohnke S., Moehser S., Surnov A., Kurth T., Jessberger R., Kretschmer K, & Garbe A.I. (2022). Role of Dynamic Actin Cytoskeleton Remodeling in Foxp3+ Regulatory T Cell Development and Function: Implications for Osteoclastogenesis. Frontiers in Immunology, 13, 836646.

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