title: Human CD16+ and CD16- monocyte subsets display unique effector properties in inflammatory conditions in vivo.
abstract: Two major subsets of human Mo are identified based on CD14 and CD16 expression: the classical CD16(-) Mo and the minor CD14(+)CD16(+) Mo. In vitro studies suggested distinct function and differentiation potential for each cell population. However, the in vivo relevance of these findings remains unclear. To evaluate the development and function of human Mo in an in vivo model, we transferred both Mo subpopulations into the peritoneum of immunocompromised mice in homeostatic or inflammatory conditions. Inflammation was induced with soluble LPS or particulate zymosan. CD16(+) were more phagocytic and produced higher amounts of TNF and IL-6 than CD16(-) Mo early after transfer with zymosan. They also produced higher levels of β2-defensin in any condition evaluated, which could represent a new marker for this subpopulation. In contrast, differentiating CD16(-) Mo (24 h after transfer) acquired greater APC capacity in LPS-induced peritonitis, whereas none of the Mo subsets attained this ability with zymosan. CX(3)CL1 supported the survival of both Mo subsets in vivo. Similar Mo subpopulations were present in human peritonitis. These results support the idea of specialized roles of the Mo subset, where CD16(+) might act in an immediate innate immune response, whereas CD16(-) could have a major role as APCs.
authors.affiliation: Department of Molecular Biomedicine, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional(CINVESTAV-IPN), Mexico City, Mexico.
authors.forename: Sergio R
authors.initials: SR
authors.lastname: Aguilar-Ruiz
authors.forename: Honorio
authors.initials: H
authors.lastname: Torres-Aguilar
authors.forename: Érika
authors.initials: É
authors.lastname: González-Domínguez
authors.forename: Juana
authors.initials: J
authors.lastname: Narváez
authors.forename: Gabriela
authors.initials: G
authors.lastname: González-Pérez
authors.forename: Germán
authors.initials: G
authors.lastname: Vargas-Ayala
authors.forename: Marco A
authors.initials: MA
authors.lastname: Meraz-Ríos
authors.forename: Eduardo A
authors.initials: EA
authors.lastname: García-Zepeda
authors.forename: Carmen
authors.initials: C
authors.lastname: Sánchez-Torres
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D058851:GPI-Linked Proteins / Q000096:biosynthesis / Q000378:metabolism; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D018836:Inflammation Mediators / Q000502:physiology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D051379:Mice; D016513:Mice, SCID; D009000:Monocytes / Q000276:immunology* / Q000473:pathology* / Q000637:transplantation; D010538:Peritonitis / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D017452:Receptors, IgG / Q000096:biosynthesis* / Q000378:metabolism; D015054:Zymosan / Q000494:pharmacology
chemical_list: C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D017452:Receptors, IgG; D015054:Zymosan