title: Influence of the lpr environment on the lymph node cell phenotypes in C57BL/6 nubg and nulpr chimeras.
abstract: Mice homozygous for the lpr gene show a marked lymphoproliferative syndrome. Most T cells which accumulate in their lymphoid organs belong to a fairly unusual subpopulation. Although being CD44+ T cells expressing neither CD4 nor CD8, they are CD3 T-cell receptor (TCR) alpha beta positive and express both Thy-1 and B220, the B-cell form of the CD45 marker. To support engraftment and development of transferred lpr lymphomyeloid cells, athymic recipients must be genetically lpr. While nude/beige (nubg) recipients do not allow the development of any lymphoproliferative syndrome, this is variable in nude/lpr (nulpr) recipients, and the genotypic origin of the proliferating lymphocytes in nulpr recipients is unclear. In this study, the surface phenotype of lymph node cells from nulpr recipients of lpr grafts ([lpr-->nulpr] chimeras) was analysed by flow cytometry, and compared with various chimeras and parental (donor and recipient) strains as controls. Abnormal cells of the lpr type were not detectable either in [lpr-->nubg] chimeras or in [wild-->nubg] controls. Absence of lpr cells was also seen in neonatal lpr thymus-grafted nubg mice engrafted previously with lpr haematopoietic cells. In contrast, a substantial emergence of double-positive B220+ Thy-1+ cells occurred in [lpr-->nulpr] chimeras, together with high levels of CD4+ cells, a substantial fraction of which might express B220. Finally, in thymus-grafted nulpr mice, the levels of B220+ Thy-1+ cells were as high as in lpr mice and there was again an expansion of CD4+ (potentially B220+) cells. Abnormality of the nulpr haemopoietic environment was also shown by the low percentages of T cells, particularly CD8+ cells, in short-lived [wild-->nulpr] chimeras. Taken together, our results underline the differences between the nubg and nulpr environments.
authors.affiliation: Laboratoire d'Immunologie, Université de Strasbourg, Illkirch, France.
authors.forename: F
authors.initials: F
authors.lastname: Tiberghien
authors.forename: R
authors.initials: R
authors.lastname: Ceredig
authors.forename: F
authors.initials: F
authors.lastname: Loor
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology*; D016026:Bone Marrow Transplantation; D016130:Immunophenotyping; D008198:Lymph Nodes / Q000276:immunology*; D008232:Lymphoproliferative Disorders / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008819:Mice, Nude; D009154:Mutation; D013045:Species Specificity; D013154:Spleen / Q000637:transplantation; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D013950:Thymus Gland / Q000637:transplantation; D018183:Transplantation Chimera / Q000276:immunology*