Bone marrow transfers in X-irradiated mice congenic at the lpr locus: some paradoxical effects.
MRL/l mice, which are homozygous at the lpr locus, can be inhibited in lpr phenotype expression (lymphadenopathy, accelerated death) by a transfer of MRL/n bone marrow cells following X-irradiation of the recipients (MRL/n bone marrow----X-irradiated MRL/l chimeras). Female MRL/l bone marrow----X-irradiated MRL/l chimeras express the lpr phenotype with a delay corresponding to the age at the time of cell transfer. However, the equivalent male chimeras resemble MRL/n bone marrow----X-irradiated MRL/l chimeras. When the reverse MRL/l bone marrow----X-irradiated MRL/n chimeras are constructed, one finds that whichever the sex is, the chimeras undergo a wasting disease looking like a graft-versus-host disease, with particularly a marked atrophy of the spleen. A similar GVH like disease is observed with C57Bl/6 lpr bone marrow----X-irradiated C57Bl/6 normal mice. These animals survive at least 5 months but manifest a spleen aplasia. When reconstituted with MRL/n bone marrow, MRL/l recipients develop higher levels of antinuclear and anti-ds/ss DNA antibodies than MRL/n recipients. This suggests that the 'lpr environment' of the host may have an influence on the development of B cell hyperactivity.
Mosbach-Ozmen
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Laboratoire d'Immunologie, Université Louis Pasteur, Strasbourg, France.
Loor
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D000818:Animals; D001327:Autoimmune Diseases / Q000209:etiology* / Q000517:prevention & control; D016026:Bone Marrow Transplantation; D005260:Female; D006086:Graft vs Host Disease / Q000209:etiology; D008232:Lymphoproliferative Disorders / Q000209:etiology* / Q000517:prevention & control; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D011828:Radiation Chimera; D014184:Transplantation, Homologous