title: T-B collaboration in the in vitro anti-Sm autoantibody response of MRL/Mp-lpr/lpr mice.
abstract: Spontaneous production of autoantibodies to the Sm nuclear Ag is highly specific for SLE and the SLE-prone MRL mouse strains. Our previous studies have demonstrated that in vitro anti-Sm production in MRL/1pr mice requires the presence of T cells. In the present investigation, these T cells were found to express the L3T4+/Lyt-2- phenotype, unlike the aberrant L3T4-/Lyt-2-"double negative" 1pr T cells, and to utilize the L3T4 determinant in generating help for the anti-Sm response. The generation of anti-Sm did not require the presence of Sm-specific Th cells, as help could also be provided by T cells activated to an irrelevant Ag, or by nonspecific factors such as IL-2. There was no evidence for suppressor cell regulation of anti-Sm, even in animals negative for this specificity. These studies indicate that ongoing production of anti-Sm in MRL/1pr mice is dependent on the presence of T cells with a normal mature surface phenotype, and that these cells act in part through the elaboration of lymphokines. They further show that the anti-Sm status of individual MRL/1pr mice is not due to the action of suppressor cells. Because T cells appear to act primarily in a permissive fashion for the anti-Sm response, it is likely that events underlying the initial generation of Sm-specific B cell precursors are critical in determining whether an individual animal develops the Sm serologic specificity. Once these cells have arisen, clonal expansion of Sm-specific B cells may proceed in the presence of activated T cells or some of their products.
authors.affiliation: Department of Medicine, University of North Carolina, Chapel Hill 27599-7280.
authors.forename: E W
authors.initials: EW
authors.lastname: Shores
authors.forename: R A
authors.initials: RA
authors.lastname: Eisenberg
authors.forename: P L
authors.initials: PL
authors.lastname: Cohen
mesh_terms: D000818:Animals; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis / Q000276:immunology; D001323:Autoantibodies / Q000096:biosynthesis*; D001324:Autoantigens / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology*; D007376:Interleukin-2 / Q000502:physiology; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D008213:Lymphocyte Activation; D008211:Lymphocyte Cooperation; D008222:Lymphokines / Q000502:physiology; D051379:Mice; D008817:Mice, Mutant Strains; D017411:Ribonucleoproteins, Small Nuclear; D013601:T-Lymphocytes / Q000276:immunology*; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D055517:snRNP Core Proteins
chemical_list: D000945:Antigens, Differentiation, T-Lymphocyte; D001323:Autoantibodies; D001324:Autoantigens; D007376:Interleukin-2; D008222:Lymphokines; D017411:Ribonucleoproteins, Small Nuclear; D055517:snRNP Core Proteins