Expression and sequences of T cell receptor beta-chain variable genes in the enlarged lymph nodes of C57BL/6-lpr/lpr mice
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Updated: Aug 8, 2026

Retroviral Transduction of Bone Marrow Progenitor Cells to Generate T-cell Receptor Retrogenic Mice
Published on: July 11, 2016
S Ohga1, Y Yoshikai, K Kishihara
1Department of Immunology, Kyushu University, Fukuoka, Japan.
Abstract:
An autosomal recessive gene, lpr, is responsible for lymphoproliferation and autoimmunity of lpr-mice, in which background genes are also known to influence the development of autoimmune disease. To define the differences in abnormally proliferating T cells between C57BL/6-lpr/lpr and MRL/Mp-lpr/lpr mice, and to try and understand the influence of background in the differing expression of autoimmune disease in both strains, we analysed the sequences of T cell antigen receptor V beta genes expressed in the cells from the enlarged lymph nodes of C57BL/6-lpr/lpr mice. Eleven beta cDNAs out of the 38 C beta-specific cDNAs contained sequences with open reading frames from the beginning of the variable region to the expected termination codons at the end of the constant regions. Notably, 36% of the functional beta-chain mRNAs expressed V beta 8.3 genes, whereas V beta 8.1 and V beta 8.2 genes were not found. These results are consistent with a relatively lower frequency of the V beta 8.1 or V beta 8.2 expressing cells in the hypertrophic lymph nodes of C57BL/6-lpr/lpr mice, detected by KJ16-133 monoclonal antibody. Interestingly, other V beta genes expressed in these mice were completely distinct from those in MRL/Mp-lpr/lpr mice as described by Singer et al. (1986). The different distribution of V beta genes expressed in C57BL/6-lpr/lpr from that in MRL/Mp-lpr/lpr mice might be related to the differences in the genetic background and the expression of lpr gene-associated autoimmunity.
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