A mouse model that is immunologically tolerant to reporter and modifier proteins
Reporter proteins have become an indispensable tool in biomedical research. However, exogenous introduction of these reporters into mice poses a risk of rejection by the immune system. Here, we describe the generation, validation and application of a multiple reporter protein tolerant ‘Tol' mou...
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| Vydáno v: | Communications biology Ročník 3; číslo 1; s. 273 |
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| Hlavní autoři: | , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
London
Nature Publishing Group UK
29.05.2020
Nature Publishing Group |
| Témata: | |
| ISSN: | 2399-3642, 2399-3642 |
| On-line přístup: | Získat plný text |
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| Shrnutí: | Reporter proteins have become an indispensable tool in biomedical research. However, exogenous introduction of these reporters into mice poses a risk of rejection by the immune system. Here, we describe the generation, validation and application of a multiple reporter protein tolerant ‘Tol' mouse model that constitutively expresses an assembly of shuffled reporter proteins from a single open reading frame. We demonstrate that expression of the
Tol
transgene results in the deletion of CD8
+
T cells specific for a model epitope, and substantially improves engraftment of reporter-gene transduced T cells. The Tol strain provides a valuable mouse model for cell transfer and viral-mediated gene transfer studies, and serves as a methodological example for the generation of poly-tolerant mouse strains.
Bresser and Dijkgraaf et al. develop the ‘Tol’ strain, a genetically modified mouse model that expresses a range of shuffled reporter and modifier proteins from a single open reading frame. This strain is immunologically tolerant to these reporter and modifier proteins, providing a valuable model system for cell transfer studies and virus-mediated gene transfer studies. |
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| Bibliografie: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
| ISSN: | 2399-3642 2399-3642 |
| DOI: | 10.1038/s42003-020-0979-0 |