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Mhcii mice

Manufactured by Jackson ImmunoResearch
Sourced in Montenegro

MHCII−/− mice are genetically engineered mice that lack the major histocompatibility complex class II (MHC II) genes. This genetic modification results in the absence of MHC II molecules, which are essential for the activation of CD4+ T cells. These mice are a valuable tool for researchers studying immune system function and disease models.

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7 protocols using mhcii mice

1

Aging and Parabiosis in Mouse Models

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All the mice used in the current study were derived from the C57BL/6 background. Retired breeder female mice (middle-aged) were purchased from Taconic. GFP-transgenic mice contained a GFP transgene under the control of the β-actin promoter (37 (link)). Red Fluorescent Protein (RFP)-transgenic mice contained a CAG promoter driving RFP inserted into the Rosa locus (38 (link)). Aged mice for parabiosis experiments (21–23 months) were obtained from the National Institute of Aging. Young CD45.1 and CD45.2 C57BL/6 mice, as well as MHCII−/− mice were obtained from the Jackson Laboratory. All mice were housed in the Joslin Diabetes Center animal facility. The Joslin Institutional Animal Care and Use Committee approved all experimental protocols involving mice.
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2

Transgenic Mouse Breeding for TCR Studies

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P25TCR-Tg30 (link) mice were bred into a C57BL/6 (CD45.1) background. C7TCR-Tg47 (link) mice have been described previously. C57BL/6 (CD45.2) and MHC-II/ mice were purchased from The Jackson Laboratory. The New York University School of Medicine Institutional Animal Care and Use Committee approved all work with animals.
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3

Genetically Modified Murine Models

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C57BL6 mice were bred in our animal facility. MHCI-restricted OTI+Rag-/- (chicken ovalbumin 257-264 peptide specific) and P14+Rag-/- (lymphocytic choriomeningitis virus (LCMV) GP33-41 peptide specific)) transgenic mice were obtained from Nathalie Labrecque and Heather Melichar (Centre de Recherche Hopital Maisonneuve-Rosemont (CRHMR)). MHCII-/- mice were obtained from The Jackson Laboratory. All TCR transgenic mice were Rag-deficient unless mentioned otherwise. OTI mice expressing constitutively active LckY505F or Thpok transgene were described previously (40 (link)). Mice were genotyped by peripheral blood analysis and/or PCR of genomic DNA isolated from an ear punch. Lymphoid organs from 5–8 week old mice were harvested for all analyses. All mice were housed under specific pathogen free conditions at the CRHMR. Animal experimentation protocols were approved by the CRHMR animal care committee and performed in accordance with the Canadian Committee for Animal Care.
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4

Generating Transgenic and Knockout Mice

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Wildtype C57BL/6 (B6) mice and MHC class II deficient (MHC-II-/-) mice were obtained from The Jackson Laboratory (Bar Harbor, ME). MyD88-/- mice were obtained from Mutant Mouse Resource and Research Centers. Jα18(-10)-/- mice (hereafter referred to as Jα18-/- mice) were generated on the B6 background in Dr. Laurent Gapin’s lab (University of Colorado) (27 (link)). We backcrossed these Jα18-/- mice to B6 mice in our mouse colony to generate wild-type littermate controls. CD1d-/- mice were generated in house and have been backcrossed onto B6 background for at least 12 generations (28 (link)). MR1-/- mice were provided by Dr. Ted Hansen (Washington University) and backcrossed to B6 mice to generate MR1+/+ littermate controls. Vα3.2+Vβ9+ CD1d-autoreactive transgenic mice (24αβ) were provided by Dr. Suzanna Cardell (University of Gothenburg) (29 (link)). MHC-II-/-CD1d-/- mice were generated by crossing CD1d-/- mice and MHC-II-/- mice. Naïve mice were housed in a specific pathogen-free facility.
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5

Utilization of Transgenic Mouse Models

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ESAT-6 TCRtg (C7) mice were provided by E. Pamer and have been described previously (9 (link)). OT-II mice were provided by M. Gerner (University of Washington). C57BL/6 and MHCII−/− mice were purchased from Jackson Laboratories (Bar Harbor, ME). All mice were housed in specific pathogen-free conditions at Seattle Children’s Research Institute (SCRI). Experiments were performed in compliance with the SCRI Animal Care and Use Committee. Both male and female mice between the ages of 8-12 weeks were used.
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6

ID93 Vaccine Efficacy in Murine Models

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Female wt C57BL/6 mice, μMT-/- (B cell deficient), CD45.1+, CD90.1+, and MHC-II-/- mice, 6-10 weeks of age, were purchased from The Jackson Laboratory. All strains were on the C57BL/6 background. Mice were immunized by i.m. injection with either saline or ID93 (a recombinant fusion protein comprised of Rv3619, Rv1813, Rv3620, and Rv2608) formulated with the adjuvant GLA-SE to provide a final vaccine dose of 0.5μg ID93 and 5μg GLA-SE [21 ]. All animals were housed in the IDRI animal care facility (Seattle, WA) under specific pathogen-free conditions. All animal experiments and protocols used in this study were approved by IDRI's Animal Care and Use Committee (ACUC).
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7

LCMV Infection in Transgenic Mice

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C57BL/6 mice, CD45.1 + , Foxp3 GFP+ transgenic (Oukka, 2007) , SMARTA TCR transgenic (Oxenius et al., 1998) , TCRb -/- (Mombaerts et al., 1992) , and MHCII -/-mice (Madsen et al., 1999) were purchased from Jackson Laboratories (Bar Harbor, ME) and bred in-house. All mice were on a B6 background and used for experiments at 6-12 weeks of age. Animal housing, care and research were in accordance with the Guide for the Care and Use of Laboratory Animals and all procedures performed were approved by the McGill University, Maisonneuve-Rosemont Hospital Research Center, Radboud University, or NIAID Animal Care Committee. For in vivo infections, LCMV-Armstrong (LCMV) was propagated as previously described (Slifka and Whitton, 2001 ) and mice infected with 2x10 5 plaque forming units (PFU) by intra-peritoneal injection (Wherry et al., 2003) . Cellular responses were assessed 8 days post-infection.
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