The DOI matches its Crossref record; 26 of the 26 references it cites were found in a registry or an index.
Mice lacking all conventional MHC class II genes
Open accessAbstract
MHC class II (MHC-II) molecules play a central role in the selection of the T cell repertoire, in the establishment and regulation of the adaptive immune response, and in autoimmune deviation. We have generated knockout mice lacking all four of the classical murine MHC-II genes (MHCII Δ/Δ mice), via a large (80-kilobase) deletion of the entire class II region that was engineered by homologous recombination and Cre recombinase-mediated excision. These mice feature immune system perturbations like those of Aα and Aβ knockout animals, notably a dearth of CD4+lymphocytes in the thymus and spleen. No new anatomical or physiological abnormalities were observed in MHCII Δ/Δ mice. Because these animals are devoid of all classical MHC-II chains, even unpaired chains, they make excellent recipients for MHC-II transgenes from other species, avoiding the problem of interspecies cross-pairing of MHC-II chains. Therefore, they should be invaluable for engineering “humanized” mouse models of human MHC-II-associated autoimmune disorders.
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Cites
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Mice lacking MHC class II molecules
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Deenick, E. K., Chan, A., Ma, C. S., Gatto, D., Schwartzberg, P. L., Brink, R., & Tangye, S. G. (2010) · Immunity · doi:10.1016/j.immuni.2010.07.015 · Cited by 347
Metadata
- Authors
- Madsen, L., Labrecque, N., Engberg, J., Dierich, A., Svejgaard, A., Benoist, C., Mathis, D., & Fugger, L.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1999-08-31
- Volume
- 96
- Issue
- 18
- Pages
- 10338-10343
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2007027030
- Cited by
- 330
- References
- 26
- FWCI
- 1.60
- Type
- journal article
- Language
- en
- Open access
- green
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- Madsen, L., Labrecque, N., Engberg, J., Dierich, A., Svejgaard, A., Benoist, C., Mathis, D., & Fugger, L. (1999). Mice lacking all conventional MHC class II genes. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.96.18.10338
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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