IL-2 receptor expression in autoimmune MRL-lpr/lpr mice. The expanded L3T4-, Lyt-2- population does not express p75 and cannot generate functional high-affinity IL-2 receptors.
Autoimmune MRL-lpr/lpr mice develop an SLE-like disease characterized by a profound lymphadenopathy within an L3T4-, Lyt-2- (DN), B220+ T-cell population. Despite its immature phenotype this subset expresses mature alpha beta TCR belonging predominantly to the V beta 8 gene family and appears to be identical to an activated form of a minor T cell population present in both the thymus and periphery of normal mice. However, the mechanisms underlying the greatly increased cellularity in lpr/lpr-bearing mice are not understood. In this study, the IL-2R expression of lpr/lpr T cells was examined to assess the contribution of IL-2-mediated division to their expansion. The lpr/lpr DN T cells lacked high-affinity IL-2R, even after stimulation, suggesting that IL-2-dependent proliferation plays no role in the expansion of these cells and demonstrating the existence of this unusual T cell phenotype in vivo.
Rosenberg
Y J
YJ
Institute of Cellular and Molecular Oncology, New York.
Nurse
F
F
Begley
C G
CG
D000818:Animals; D000945:Antigens, Differentiation, T-Lymphocyte; D000950:Antigens, Ly; D001327:Autoimmune Diseases / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D002478:Cells, Cultured; D002999:Clone Cells / Q000145:classification / Q000276:immunology / Q000378:metabolism; D007153:Immunologic Deficiency Syndromes / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D008213:Lymphocyte Activation; D008565:Membrane Proteins / Q000378:metabolism*; D051379:Mice; D008817:Mice, Mutant Strains; D008970:Molecular Weight; D010641:Phenotype; D015375:Receptors, Interleukin-2 / Q000172:deficiency / Q000378:metabolism*; D013601:T-Lymphocytes / Q000145:classification / Q000276:immunology / Q000378:metabolism*
D000945:Antigens, Differentiation, T-Lymphocyte; D000950:Antigens, Ly; D008565:Membrane Proteins; D015375:Receptors, Interleukin-2