ArticleThe Journal of experimental medicine1992
Analysis of a T cell receptor gene as a target of the somatic hypermutation mechanism.
Article in The Journal of experimental medicine, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 34 citations in OpenAlex.
- Lost structural and functional inter-relationships between Ig and TCR loci in mammals revealed in sharks.Immunogenetics · 2021Review
- Complex regulation of somatic hypermutation by cis-acting sequences in the endogenous IgH gene in hybridoma cells.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- lambda 5, but not mu, is required for B cell maturation in a unique gamma 2b transgenic mouse line.The Journal of experimental medicine · 1995Article
- Somatic hypermutation of an immunoglobulin mu heavy chain transgene.The Journal of experimental medicine · 1993Article
- Evidence for an alpha/beta T cell-independent mechanism of resistance to mycobacteria. Bacillus-Calmette-Guerin causes progressive infection in severe combined immunodeficient mice, but not in nude mice or in mice depleted of CD4+ and CD8+ T cells.The Journal of experimental medicine · 1992Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
In an effort to identify cis-acting elements required for targeting of the somatic hypermutation process in mice, we examined whether a T cell receptor (TCR) transgene under the control of the immunoglobulin (Ig) heavy (H) chain intron enhancer would be mutated in antigen-stimulated B cells. Hybridomas were established from splenic B cells of mice carrying two copies of the TCR transgene after hyperimmunization with phosphorylcholine keyhole limpet hemocyanin. Northern analysis revealed that all of the transgene-containing hybridomas expressed the TCR mRNA. Multiple somatic point mutations were found in seven of eight endogenous Ig VH genes examined. In contrast, 29 of 32 TCR genes examined contained no mutations. One potential mutation was seen in each of the three other TCR genes. Our data indicate that although the TCR transgene is expressed in B cells, it is not efficiently targeted by the mutator mechanism. Furthermore, the presence of an Ig H chain enhancer is itself not sufficient for targeting of the somatic hypermutation mechanism.
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