| First Author | Radl J | Year | 1979 |
| Journal | J Immunol | Volume | 122 |
| Issue | 2 | Pages | 609-13 |
| PubMed ID | 368243 | Mgi Jnum | J:265416 |
| Mgi Id | MGI:6200872 | Doi | 10.4049/jimmunol.122.2.609 |
| Citation | Radl J, et al. (1979) Idiopathic paraproteinemia. II. Transplantation of the paraprotein-producing clone from old to young C57BL/KaLwRij mice. J Immunol 122(2):609-13 |
| abstractText | Transplantation experiments in the C57BL/KaLwRij mouse model of idiopathic paraproteinemia (IP) showed that an IP-producing clone can be further propagated in young, lethally irradiated mice and also equally as well in nonirradiated recipients by a bone marrow and/or spleen cell transfer. The latency period before the original paraprotein was detected in the sera of recipients varied in different experiments between 1 and 9 months after transplantation. With subsequent transplantations, the "take" frequency gradually decreased. Propagation of IP for three to four generations seems to be the final limit. In comparison to age-matched seems to be the final limit. In comparison to age-matched control groups, no substantial influence of the transplanted IP on the survival of the recipients was observed. In contrast, transplantation of cells from mice with a B cell lymphoma or a myeloma led to continuous propagation of the malignancy, with a high "take" frequency, progressive development of the paraproteinemia, and a shortened survival time of the recipients. These findings indicate that IP represents in its final stage in the aging C57BL mice an intrinsic cellular defect within the affected B cell clone, which is, however, different from that found in B cell malignancies. |
