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dc.contributor.author | Cortegano, Isabel | |
dc.contributor.author | Martinez-Carrascoso, Isabel | |
dc.contributor.author | Prado-Zamora, Maria Carmen | |
dc.contributor.author | Ruíz, Carolina | |
dc.contributor.author | Hortigüela, Rafael | |
dc.contributor.author | Alia, Mario | |
dc.contributor.author | Vilar, Marçal | |
dc.contributor.author | Mira, Helena | |
dc.contributor.author | Cano, Eva | |
dc.contributor.author | Dominguez-Rodriguez, Mercedes | |
dc.contributor.author | Andres, Belen de | |
dc.contributor.author | Gaspar, Maria Luisa | |
dc.date.accessioned | 2019-02-20T10:37:10Z | |
dc.date.available | 2019-02-20T10:37:10Z | |
dc.date.issued | 2017-08-17 | |
dc.identifier.citation | Cell Death Dis. 2017 Aug 17;8(8):e3000. | es_ES |
dc.identifier.issn | 2041-4889 | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/7189 | |
dc.description.abstract | Aging has a strong impact on the activity of the immune system, enhancing susceptibility to pathogens and provoking a predominant pre-inflammatory status, whereas dampening responses to vaccines in humans and mice. Here, we demonstrate a loss of marginal zone B lymphocytes (MZ, CD19+CD45R+CD21++CD23lo) and a decrease of naive B cells (CD19+IgD+), whereas there is an enhancement of a CD19+CD45Rlo innate-like B cell population (B1REL) and the so-called aged B cell compartment (ABC, CD45R+CD21loCD23loCD5-CD11b-) in aged senescence-accelerated (SAMP8) mice but not in aged senescence-resistant (SAMR1) mice. These changes in aged SAMP8 mice were associated with lower IgG isotype levels, displaying low variable gene usage repertoires of the immunoglobulin heavy chain (VH) diversity, with a diminution on IgG1-memory B cells (CD11b-Gr1-CD138-IgM-IgD-CD19+CD38+IgG1+), an increase in T follicular helper (TFH, CD4+CXCR5+PD1+) cell numbers, and an altered MOMA-1 (metallophilic macrophages) band in primary follicles. LPS-mediated IgG1 responses were impaired in the B1REL and ABC cell compartments, both in vitro and in vivo. These data demonstrate the prominent changes to different B cell populations and in structural follicle organization that occur upon aging in SAMP8 mice. These novel results raise new questions regarding the importance of the cellular distribution in the B cell layers, and their effector functions needed to mount a coordinated and effective humoral response. | es_ES |
dc.description.sponsorship | This work was supported by Acción Estratégica de Salud Carlos III (AESI), Grant PI14/0049 and Ministerio de Economía, Industria y Competitividad (MINECO), Grant SAF2015-70880-R, Grant SAF2015-70433-R and BFU 2013-42746. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Nature Publishing Group | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.subject.mesh | Aging | es_ES |
dc.subject.mesh | Animals | es_ES |
dc.subject.mesh | Antigens, CD | es_ES |
dc.subject.mesh | B-Lymphocytes | es_ES |
dc.subject.mesh | Cell Death | es_ES |
dc.subject.mesh | Cell Proliferation | es_ES |
dc.subject.mesh | Gene Expression Regulation, Developmental | es_ES |
dc.subject.mesh | IgG Deficiency | es_ES |
dc.subject.mesh | Immunity, Humoral | es_ES |
dc.subject.mesh | Immunity, Innate | es_ES |
dc.subject.mesh | Immunoglobulin D | es_ES |
dc.subject.mesh | Immunoglobulin A | es_ES |
dc.subject.mesh | Immunoglobulin Heavy Chains | es_ES |
dc.subject.mesh | Immunoglobulin M | es_ES |
dc.subject.mesh | Immunologic Memory | es_ES |
dc.subject.mesh | Lipopolysaccharides | es_ES |
dc.subject.mesh | Mice, Inbred BALB | es_ES |
dc.subject.mesh | Mice, Transgenic | es_ES |
dc.subject.mesh | Primary Cell Culture | es_ES |
dc.subject.mesh | Signal Transduction | es_ES |
dc.subject.mesh | Spleen | es_ES |
dc.subject.mesh | T-Lymphocytes, Helper-Inducer | es_ES |
dc.title | Altered marginal zone and innate-like B cells in aged senescence-accelerated SAMP8 mice with defective IgG1 responses | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Atribución 4.0 Internacional | * |
dc.identifier.pubmedID | 28817118 | es_ES |
dc.format.volume | 8 | es_ES |
dc.format.number | 8 | es_ES |
dc.format.page | e3000 | es_ES |
dc.identifier.doi | 10.1038/cddis.2017.351 | es_ES |
dc.contributor.funder | Instituto de Salud Carlos III | |
dc.contributor.funder | Ministerio de Economía, Industria y Competitividad (España) | |
dc.description.peerreviewed | Sí | es_ES |
dc.relation.publisherversion | https://doi.org/10.1038/cddis.2017.351 | es_ES |
dc.identifier.journal | Cell death & disease | es_ES |
dc.repisalud.centro | ISCIII::Centro Nacional de Microbiología | es_ES |
dc.repisalud.centro | ISCIII::Unidad Funcional de Investigación de Enfermedades Crónicas (UFIEC) | es_ES |
dc.repisalud.institucion | ISCIII | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/PI14/0049 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/SAF2015-70880-R | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/SAF2015-70433-R | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/BFU 2013-42746 | es_ES |
dc.rights.accessRights | open access | es_ES |