title: Autoantibody production in healthy elderly people is not promoted by interleukin-10 although this cytokine is expressed in them by a peculiar CD8+CD3+ large granular cell subpopulation.
abstract: Healthy elderly people tend to have autoantibodies in their sera. These antibodies, not being associated with any clinical manifestation, have been considered as natural autoantibodies. In systemic lupus erythematosus, as well as in rheumatoid arthritis, the presence of autoantibodies characteristic of these disease (anti-dsDNA and rheumatoid factor, respectively) depends on the endogeneous production of IL-10. The same could hold true for autoantibodies found in healthy elderly individuals. In the present work, the authors analysed whether an increased production of IL-10 contributed to the production of autoantibodies in elderly people. The authors found that there is neither increased in vivo gene expression nor augmented production of IL-10 by peripheral blood mononuclear cells from elderly women even if they do produce autoantibodies. The authors further sought to determine if the production of autoantibodies is inhibited in vitro by adding an anti-IL-10 MoAb to cell cultures and found that it is not. Despite these negative findings of a role for IL-10 in the production of autoantibodies in elderly people, the authors investigated which cells produce IL-10. In so doing they found that intracellular IL-10 expression occurred exclusively in monocytes in young female controls, but in elderly females it involved also CD8+CD3+ large granular cells. These results indicate that autoantibody production in healthy aged individuals is IL-10 independent.
authors.affiliation: Department of Immunology and Rheumatology, Instituto Nacional de la Nutrición Salvador Zubirán, Mexico City, Mexico.
authors.forename: L
authors.initials: L
authors.lastname: Llorente
authors.forename: Y
authors.initials: Y
authors.lastname: Richaud-Patin
authors.forename: C
authors.initials: C
authors.lastname: Alvarado
authors.forename: A
authors.initials: A
authors.lastname: Vidaller
authors.forename: J
authors.initials: J
authors.lastname: Jakez-Ocampo
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000276:immunology*; D001323:Autoantibodies / Q000096:biosynthesis* / Q000187:drug effects*; D015415:Biomarkers / Q000032:analysis; D017252:CD3 Complex / Q000032:analysis*; D016827:CD8 Antigens / Q000032:analysis*; D005260:Female; D005786:Gene Expression Regulation / Q000276:immunology; D006801:Humans; D016130:Immunophenotyping; D016753:Interleukin-10 / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism / Q000494:pharmacology*; D016131:Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism*; D012217:Rheumatoid Factor / Q000032:analysis
chemical_list: D001323:Autoantibodies; D015415:Biomarkers; D017252:CD3 Complex; D016827:CD8 Antigens; D016753:Interleukin-10; D012217:Rheumatoid Factor