Tcrα mice

Manufactured by Jackson ImmunoResearch

TCRα−/− mice are genetically modified mice that lack the alpha chain of the T cell receptor (TCR). This genetic modification results in the absence of mature T cells in these mice. The TCRα−/− mice are commonly used as an animal model for studying T cell biology and developing immunotherapies.

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14 protocols using tcrα mice

Genetically Modified Mice for Research

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C57BL/6J mice were purchased from Japan SLC. Mcpt8^GFP (18 (link)), Rag2^−/− (19 (link)), Il3^−/− (20 (link)), and Fcer1g⁻^/⁻ (21 (link)) mice on the C57BL/6J background were described previously. OT-II Tg/Rag2^−/− mice (22 (link)) were kindly provided by Dr. Francis R. Carbone. Tcrα^−/− mice (23 (link)) were obtained from the Jackson laboratory. All mice were maintained under specific pathogen-free conditions in our animal facilities in accordance with the guidelines of the Tokyo Medical and Dental University for animal care, and all animal studies were approved by the Institution Animal Care and Use Committee of Tokyo Medical and Dental University (permit number: 0170087A).

Ohta T., Yoshikawa S., Tabakawa Y., Yamaji K., Ishiwata K., Shitara H., Taya C., Oh-hora M., Kawano Y., Miyake K., Yamanishi Y., Yonekawa H., Watanabe N., Kanuka H, & Karasuyama H. (2017). Skin CD4+ Memory T Cells Play an Essential Role in Acquired Anti-Tick Immunity through Interleukin-3-Mediated Basophil Recruitment to Tick-Feeding Sites. Frontiers in Immunology, 8, 1348.

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Immunodeficient Mouse Models for Cancer Research

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All animals were used according to protocols approved by Institutional Animal Use Committee of the University of Chicago and Aduro Biotech, Inc., and maintained in pathogen-free conditions in a barrier facility. C57BL/6, BALB/c, C3H/He and TCRα^−/− mice were obtained from Jackson and Charles River. RAG2^−/− mice were obtained from Taconic. Tmem173^−/− (STING-deficient) mice were provided by Dr. G. Barber (University of Miami), and STING^−/− (goldenticket) (Sauer JD, et al., 2011 (link)) and IFNAR^−/− mice were purchased from Jackson. Batf3^−/− mice were provided by Dr. Kenneth M. Murphy (Washington University School of Medicine, St. Louis, MO).

Corrales L., Glickman L.H., McWhirter S.M., Kanne D.B., Sivick K.E., Katibah G.E., Woo S.R., Lemmens E., Banda T., Leong J.J., Metchette K., Dubensky TW J.r, & Gajewski T.F. (2015). Direct activation of STING in the tumor microenvironment leads to potent and systemic tumor regression and immunity. Cell reports, 11(7), 1018-1030.

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Genetic Mouse Models for T Cell Studies

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TCRα⁻ mice were purchased from Jackson Laboratory (88 (link)). BMPR1α^T− mice were generated by crossing BMPR1α conditional knockout mice with mice expressing CD4cre and Foxp3^GFP reporter (25 (link), 89 (link), 90 (link)). Foxp3^GFP and BMPR1α^T− mice were crossed with mice expressing TCR specific for analog of peptide derived from pigeon cytochrome C (PCC) (91 (link)). All mice were on the C57BL6 genetic background. Mice were bred and housed in specific pathogen-free conditions in the animal facility of Old Dominion University. All experiments were approved by IACUC. Both female and male mice were used in experiments and we have not observed any difference in T cell development and activation between sexes. Mice were 6- to 12-week-old for all experiments.

Browning L.M., Pietrzak M., Kuczma M., Simms C.P., Kurczewska A., Refugia J.M., Lowery D.J., Rempala G., Gutkin D., Ignatowicz L., Muranski P, & Kraj P. (2018). TGF-β–mediated enhancement of TH17 cell generation is inhibited by bone morphogenetic protein receptor 1α signaling. Science signaling, 11(545), eaar2125.

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Transgenic Malaria Parasite Generation

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Male and female C57BL/6 wild type, Tbx21^−/−, Rag1^−/− and Tcrα^−/− mice (6–8 weeks, 16–21g) were purchased from Jackson Laboratories. SMARTA mice were generously provided by Dorian McGavern (Scripps) via Allan Zajac (UAB). The University of Oklahoma Health Sciences Center and University of Iowa Institutional Animal Care and Use Committees approved all experiments. Plasmodium yoelii (clone 17XNL, BEI Resources/MR4/ATCC) was inoculated into mice intravenously. To generate the T cell epitope tagged transgenic parasites (see Fig. S1 and Table S1), a dispensable genetic locus (“p230p”) was stably targeted with an expression cassette of Hep17 protein tagged with the GP_61–80 CD4 T cell epitope (amino acids 61–80 from LCMV glycoprotein). Standard methods (Jongco et al., 2006 (link), Lindner et al., 2013 (link)) were used to create and integrate a linearized pDEF construct, select transgenic parasites, and obtain two pure, clonal populations. Parasitemia was measured using flow cytometry as previously described (Malleret et al., 2011 (link)). LCMV clone 13 (2×10⁶ plaque forming units) was administered i.p. 50 µg of rIgG or α-OX40 antibody (clone OX86, BioXCell) were administered i.p. on the days indicated in figure legends.

Zander R.A., Vijay R., Pack A.D., Guthmiller J.J., Graham A.C., Lindner S.E., Vaughan A.M., Kappe S.H, & Butler N.S. (2017). Th1-like Plasmodium-specific memory CD4+ T cells unexpectedly support humoral immunity. Cell reports, 21(7), 1839-1852.

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Transgenic Mouse Strains for NKT Cell Research

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B6, CD45.1 congenic B6 mice, Vα14-Jα18 transgenic (Vα14Tg) mice, TCR-α^−/− mice, and Lck^pr-Bcl-xL Tg mice were purchased from The Jackson Laboratory. Vα14Tg mice were crossed with TCR-α^−/− to generate Vα14TgTCR-α^−/− mice. Uqcrfs1^fl/fl;CD4-Cre⁺ (T- Uqcrfs1^−/−) and Uqcrfs1^fl/fl on B6 background were generated as described previously (5 (link)). Jα18^−/− mice on B6 background were provided by Luc Van Kaer, Vanderbilt University, Nashville, TN. All animal work was approved by the Northwestern University Institutional Animal Care and Use Committee.

Weng X., Kumar A., Cao L., He Y., Morgun E., Visvabharathy L., Zhao J., Sena L.A., Weinberg S.E., Chandel N.S, & Wang C.R. (2021). Mitochondrial metabolism is essential for invariant natural killer T cell development and function. Proceedings of the National Academy of Sciences of the United States of America, 118(13), e2021385118.

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Generation and Characterization of Mouse Models

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Wild type (WT) C57BL/6 (B6) mice were obtained from Frederick Cancer Research Facility (Frederick, MD). Mice expressing p38αβ^Y323F, in which endogenous p38α and p38β contain a Tyr -> Phe substitution at residue 323 (double knockin, or DKI mice)^{13 (link)}, were crossed onto the B6 background for at least 12 generations. TCRα^−/− mice were obtained from Jackson Laboratories. Healthy eight to twelve week old age and sex matched mice were used for experiments. To obtain KPC mice, conditional LSL-Trp53^R172H/+ LSL-Kras^G12D/+ were interbred with Pdx-1-Cre mice to yield LSL-Kras^G12D/+;LSL-Trp53^R172H/+;Pdx-1-Cre triple mutant animals. Mice were maintained in the National Cancer Institute pathogen-free facility. All animal experiments were performed under animal study protocols approved by the National Cancer Institute Animal Care and Use Committee.

Alam M.S., Gaida M.M., Bergmann F., Lasitschka F., Giese T., Giese N.A., Hackert T., Hinz U., Hussain S.P., Kozlov S.V, & Ashwell J.D. (2015). Selective inhibition of the p38 alternative activation pathway in infiltrating T cells inhibits pancreatic cancer progression. Nature medicine, 21(11), 1337-1343.

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Murine Immune Response Protocols

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C57BL/6 and TCRα^−/− mice (29 (link)) were purchased from Jackson Laboratories. Mice were raised in a specific pathogen-free environment at the University of Colorado Anschutz Medical campus. All animal procedures were approved by the University of Colorado Institutional Animal Care and Use Committees (protocol 00065) and were carried out in accordance with the approved guidelines.

Krovi S.H., Kappler J.W., Marrack P, & Gapin L. (2019). Inherent reactivity of unselected TCR repertoires to peptide-MHC molecules. Proceedings of the National Academy of Sciences of the United States of America, 116(44), 22252-22261.

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Characterization of TCR and PD-1 Knockout Mice

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Mice 6 to 10 weeks of age were used for all experiments. Wild-type (WT) C57BL/6 mice and TCRα^−/− mice were purchased from the Jackson Laboratory. P14 TCR transgenic (Tg) were purchased from Jackson Lab and Pdcd1^−/− mice (developed in Dr. Arlene Sharpe's lab) have been previously described (32, 33 (link)). All experimental mice were housed in specific pathogen–free conditions and used in accordance with animal care guidelines from the Harvard Medical School Standing Committee on Animals, Dana-Farber Cancer Institute, and the NIH. Animal protocols were approved by the Harvard Medical School Standing Committee on Animals.

Bu X., Juneja V.R., Reynolds C.G., Mahoney K.M., Bu M.T., McGuire K.A., Maleri S., Hua P., Zhu B., Klein S.R., Greenfield E.A., Armand P., Ritz J., Sharpe A.H, & Freeman G.J. (2021). Monitoring PD-1 Phosphorylation to Evaluate PD-1 Signaling during Antitumor Immune Responses. Cancer Immunology Research, 9(12), 1465-1475.

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Diverse Mouse Strains for Immunology Research

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C57Bl/6J, CAG-ECFP, CAG-DsRed and TCRα^−/− mice were purchased from Jackson Laboratories. OT-II Rag-1^−/− mice were purchased from Taconic. CD11c-EYFP mice were a kind gift from Dr. Michel C. Nussenzweig (The Rockefeller University, NY) (21 (link)). NJ.1638 mice were obtained from the Laboratories of Drs. Nancy and Jamie Lee (Mayo Clinic, AZ) (22 (link)). IL-13 DsRed mice were kindly provided by Dr. William Paul (NIAID, NIH) (23 (link)). Both male and female mice were used at 6-12 weeks of age; mice in different experimental groups were matched for age and sex. Animals were maintained at the Central Animal Laboratory of the University of Turku or at an Association for Assessment and Accreditation of Laboratory Animal Care- accredited animal facility at NIAID. All animal procedures were approved by the Ethical Committee for Animal Experimentation in Finland and/or the Animal Care and Use Committee, NIAID, NIH. They were done in adherence with the rules and regulations of the Finnish Act on Animal Experimentation (62/2006) and were performed according to the 3R-principle (animal license number 5588/04.10.07/2014).

Veres T.Z., Kopcsányi T., van Panhuys N., Gerner M.Y., Liu Z., Rantakari P., Dunkel J., Miyasaka M., Salmi M., Jalkanen S, & Germain R.N. (2016). Allergen-induced CD4+ T-cell cytokine production within airway mucosal DC-T-cell clusters drives the local recruitment of myeloid effector cells. Journal of immunology (Baltimore, Md. : 1950), 198(2), 895-907.

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Murine Autoimmune Encephalomyelitis Model

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C57BL/6NCr (WT) mice were purchased from the National Cancer Institute, while MOG KO mice66 (link) were a gift from Hugh Reid and were bred on site. Thy1.1+, Nur77^gfp and TCRα−/− mice were purchased from Jackson Laboratories and were bred on site. Mice were 6–8 weeks old when used for experiments. Both males and females were used. WT mice immunized with MOG_35–55 were monitored for weight loss due to experimental autoimmune encephalomyelitis (EAE) and were killed if weights fell <20% of initial starting weight. Experimental sample sizes were chosen from previous experiments on naive and expanded T-cell numbers8 . No mice were excluded from analysis. No randomization was performed for experiments and no investigator blinding was performed. All animals were housed in an Emory University Department of Animal Resources facility (Atlanta, GA, USA). Permission was granted and performed in accordance with the protocols of the Institutional Animal Care and Use Committee.

Martinez R.J., Andargachew R., Martinez H.A, & Evavold B.D. (2016). Low-affinity CD4+ T cells are major responders in the primary immune response. Nature Communications, 7, 13848.

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