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Recombinase‐activating gene 1‐associated expression of the myelin basic protein 1‐11‐specific transgenic T‐cell receptor in H‐2 b mice
Author(s) -
Buenafe Abigail C.,
Sherwood Courtney,
Moes Nicole,
Jones Richard E.
Publication year - 2009
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.21839
Subject(s) - recombination activating gene , biology , myelin basic protein , microbiology and biotechnology , transgene , recombinase , t cell receptor , gene , offspring , gene rearrangement , gene expression , genetics , t cell , myelin , immune system , recombination , pregnancy , neuroscience , central nervous system
We pursued a breeding strategy intended to generate disease‐resistant mice with exclusive expression of the H‐2 u ‐restricted myelin basic protein (MBP) 1‐11 peptide‐specific transgenic (Tg) T‐cell receptor (TCR) on the T‐cell‐deficient RAG1KO (H‐2 b ) background. Utilizing specific screening assays for the offspring, analyses of the F1 intercross and subsequent crosses revealed that the TgTCR‐associated clonotypic marker detected by the 3H12 mAb could be found only in association with the H‐2 b homozygous background in offspring possessing a functional rag1 gene. Moreover, expression of the MBP‐specific TgTCR could not be found in H‐2 b homozygous offspring that were RAG1 deficient ( rag1 −/− ). PCR analysis of genomic DNA from these 3H12‐negative offspring verified the presence of the TCR transgenes. Thus, the presence of a functional rag1 gene was required for the expression of the MBP‐specific TgTCR on the H‐2 b background. Given the role for RAG1, the results have important implications for T‐cell repertoire development. © 2008 Wiley‐Liss, Inc.