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Cloning of B cells from autoimmune MRL-lpr/lpr and MRL.xid mice
Authors:David S Pisetsky  Sandra A Caster  Margaret Piper  David W Scott  Alfred D Steinberg
Institution:1. Department of Medicine, Durham VA Hospital Durham, North Carolina 27705 USA;2. Divisions of Rheumatic and Genetic Diseases and Immunology, Duke University Medical Center, Durham, North Carolina 27705 USA;3. Section on Cellular Immunology, Arthritis and Rheumatism Branch, National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20205 USA
Abstract:The relationship between colony formation (cloning) of B cells and their activation in murine autoimmunity was investigated in MRL-lpr/lpr and MRL.xid mice. Cells from MRL-lpr/lpr mice showed similar requirements for in vitro growth as normal CBA/J and BALB/c cells, with maximal colony formation in the presence of the supporting factors lipopolysaccharide and sheep red blood cells. The frequency of colony-forming cells from MRL-lpr/lpr spleens or hapten-specific B-cell preparations was slightly greater than the two normal control strains, with this difference significant only for a comparison of BALB/c and MRL-lpr/lpr spleens. In contrast, MRL-lpr/lpr mice bearing the xid gene for B-cell immunodeficiency (MRL.xid) had markedly reduced B-cell colony formation. These mice nevertheless expressed anti-DNA antibodies, although at levels reduced from that of MRL-lpr/lpr controls. These results indicate that enhanced in vitro colony formation need not accompany B-cell hyperactivity in murine autoimmune disease and that autoantibody production can occur in mice with impairment in this growth property.
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