title: RANTES and MIP-1alpha production by T lymphocytes, monocytes and NK cells from nonagenarian subjects.
abstract: While numerous previous studies have investigated age-related changes of cytokine production, little is known about chemokines, the importance of which in regulating immune response is becoming increasingly evident. In this study, a group of healthy subjects over 90 years old is compared to a group of young subjects, we evaluated the ability of monocytes, T lymphocytes and NK cells: (1) to produce RANTES and MIP-1alpha, either in basal conditions or after stimulation with, respectively, LPS, anti-CD3 MoAb and IL-2; (2) to express the corresponding chemokine receptors (CCR1, CCR3, CCR5). We demonstrate that: (a) monocytes, T lymphocytes and NK cells spontaneously produced detectable amounts of chemokines, both in young and old subjects; (b) monocyte-dependent RANTES and MIP-1alpha production induced by LPS was up-regulated in nonagenarian subjects as anti-CD3-induced secretion from T cells; (c) RANTES and MIP-1alpha production by IL-2 stimulated NK cells was reduced in elderly subjects; (d) CCR1, CCR3 and CCR5 were widely expressed on monocytes, but less expressed on T lymphocytes and NK cells. The diversity within PBMC might reflect their different states of activation and/or responsiveness, influencing the ability to develop rapid innate and long-lasting adaptive immune responses.
authors.affiliation: Laboratorio di Immunologia e Genetica, Istituto di Ricerca Codivilla-Putti, IOR Bologna, Dipartimento di Medicina Interna e Gastroenterologia, University of Bologna, Via di Barbiano 1/10, 40136 Bologna, Italy. marianie@alma.unibo.it
authors.forename: Erminia
authors.initials: E
authors.lastname: Mariani
authors.forename: Lia
authors.initials: L
authors.lastname: Pulsatelli
authors.forename: Simona
authors.initials: S
authors.lastname: Neri
authors.forename: Paolo
authors.initials: P
authors.lastname: Dolzani
authors.forename: Alessandra
authors.initials: A
authors.lastname: Meneghetti
authors.forename: Tania
authors.initials: T
authors.lastname: Silvestri
authors.forename: Giovanni
authors.initials: G
authors.lastname: Ravaglia
authors.forename: Paola
authors.initials: P
authors.lastname: Forti
authors.forename: Luca
authors.initials: L
authors.lastname: Cattini
authors.forename: Andrea
authors.initials: A
authors.lastname: Facchini
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000097:blood / Q000276:immunology*; D002478:Cells, Cultured; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000096:biosynthesis*; D005260:Female; D006801:Humans; D007694:Killer Cells, Natural / Q000166:cytology / Q000187:drug effects / Q000276:immunology*; D008070:Lipopolysaccharides / Q000276:immunology / Q000494:pharmacology; D019402:Macrophage Inflammatory Proteins / Q000096:biosynthesis*; D008297:Male; D009000:Monocytes / Q000166:cytology / Q000187:drug effects / Q000276:immunology*; D054389:Receptors, CCR1; D054397:Receptors, CCR3; D019713:Receptors, CCR5 / Q000096:biosynthesis; D019707:Receptors, Chemokine / Q000096:biosynthesis; D013601:T-Lymphocytes / Q000166:cytology / Q000187:drug effects / Q000276:immunology*
chemical_list: C515300:CCR1 protein, human; C515350:CCR3 protein, human; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D008070:Lipopolysaccharides; D019402:Macrophage Inflammatory Proteins; D054389:Receptors, CCR1; D054397:Receptors, CCR3; D019713:Receptors, CCR5; D019707:Receptors, Chemokine