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  01B96 B6-LY5.2/Cr

The following strain information has been provided by Dr. Bonnie Mathieson.

B6-Ly5.2 Congenic mice are really C57B6-Ly-5a mice, expressing the Ly5.1 antigen.

According to current nomenclature the "B6-Ly5.2" congenic mice actually express the Ly5.1 antigen or the CD45a allele that was renamed about 15 years after it was first described, sometime in the late 1980's. Other studies have shown that this antigen is expressed on the common isoform of the "T200" molecule that is expressed essentially all lymphocytes and nucleated WBC's in the mouse. Because it is expressed at a very high level, even on many immature precursors, we found it useful for cell transfer experiments.

The B6-Ly5.2 congenic was derived by E.A. Boyse's group at Sloan Kettering in New York in the early 70's before the nomenclature was redefined (See Komura, K., Itakura, K., Boyse, E.A., and John, M: Ly-5: A new T-lymphocyte antigen system. Immunogenetics 1: 452-456, 1975. Scheid, M., and Triglia, D.: Further Description of the Ly-5 System. Immunogenetics 9: 423-433, 1979.) To my knowledge, the first reference to the fact that there were congenic mice is indicated in this latter paper in the materials and methods section of the paper. Ted Boyse named the alleles in the order that they were defined. Thus the antigen detected by Komura and Margaret Scheid in strain 129 mice was the #2 allele and it differed from that expressed in B6 and most other strains which carried the #1 allele. Fung-Wen Shen subsequently produced the monoclonal antibodies used to detect the allelic forms: Shen, F.-W.: Monoclonal antibodies to mouse lymphocyte differentiation antigens in Monoclonal Antibodies and T cell Hybridomas: Perspectives and Technical advances: G. Hammerling, U. Hammerling and J.F. Kearney, eds. Elsiever/North Holland and Biomedical Press, Amsterdam/ New York/Oxford, 1981, pp. 25-31.

Because of some confusion with Lyb and Lyt antigens that resulted in a couple of antigens getting the same number designation. A nomenclature committee came along and decided that everything on B6 would be the "b" or #2 allele and everything bred into the B6 background the "a" or #1 allele; For many antigens this did not make any difference, but it reversed the nomenclature of the B6-Ly5 antigen. (Morse, H.C., III, Shen, F.-W., and Hammerling, U.: Genetic Nomenclature for loci controlling mouse lymphocyte antigens. Immunogenetics 25: 71-78, 1987.)

By the time that the committee did this, the "B6-Ly5.2" mice had been backcrossed and selected nearly 20 times on the B6 background that was maintained by Ted Boyse independently from the JAX colony for more than 15 years. In the 1970's, the strain was in use in several laboratories, but not readily available. I had imported this strain directly from E.A. Boyse into the NIAID breeding colony that Ron Schwartz and I managed in Rockville in the late 1970's. When I returned from the Basel Institute in 1983, I worked with Clarence Reeder to transfer this and several other congenic stocks of mice through sterile cesarean section into the NCI colony because the mice in the NIAID colony at that time had acquired mouse hepatitis virus. Thus we had moved the mice and started breeding them at the NCI contract facility before the nomenclature was changed. Because there were only a handful of users that had learned about these mice through word of mouth, everyone learned, as they acquired the mice, that the mice carried the opposite allele to B6 and were useful for cell transfer experiments. The allele was expressed at high levels on all lymphocytes and was useful in bone marrow transplant studies and thymus and NK cell transplant studies that I was doing at the time.

Because B6 mice were readily available from the JAX, we did not attempt to import Ted Boyse's background strain. However, I did perform long-term skin grafts from the mice initially imported from Ted's group onto C57BL6 mice, that lasted more than a year on their recipients (I believe that we terminated the engrafted mice at about 500 days), indicating extensive histocompatibility.