Abnormalities induced by the mutant gene Ipr: expansion of a unique lymphocyte subset.

HC Morse 3rd, WF Davidson, RA Yetter… - … (Baltimore, Md.: 1950 …, 1982 - journals.aai.org
HC Morse 3rd, WF Davidson, RA Yetter, ED Murphy, JB Roths, RL Coffman
Journal of immunology (Baltimore, Md.: 1950), 1982journals.aai.org
Mice carrying the Ipr mutation develop massive lymphoadenopathy and severe autoimmune
disease. The characteristics of the cell population that proliferates in lymphoid tissues were
evaluated by the use of a) monoclonal antibodies and FMF, and b) molecular genetic
studies of Ig heavy chain genes. The lymph node cells of different strains of mice
homozygous for the Ipr mutation were shown to be almost uniformly Thy-1+, Ly-1+, Ly-2-, H-
11+, Ly-5+, sIg-, ThB-, 2C2+, IA-, 6B2+, and therefore to have surface characteristics of both …
Abstract
Mice carrying the Ipr mutation develop massive lymphoadenopathy and severe autoimmune disease. The characteristics of the cell population that proliferates in lymphoid tissues were evaluated by the use of a) monoclonal antibodies and FMF, and b) molecular genetic studies of Ig heavy chain genes. The lymph node cells of different strains of mice homozygous for the Ipr mutation were shown to be almost uniformly Thy-1+, Ly-1+, Ly-2-, H-11+, Ly-5+, sIg-, ThB-, 2C2+, I-A-, 6B2+, and therefore to have surface characteristics of both T and B cells. Molecular genetic studies of the arrangements of Ig heavy chain genes showed that they were not rearranged as in pre-B and B cells. These results suggest that an abnormal proliferating population of T cells in Ipr/Ipr mice aberrantly express B cell surface markers.
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