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The Role of Collectins and Galectins in Lung Innate Immune Defense

dc.contributor.authorCasals Carro, María Cristina
dc.contributor.authorCampanero-Rhodes, María
dc.contributor.authorGarcía-Fojeda García-Valdecasas, María Belén
dc.contributor.authorSolís, Dolores
dc.date.accessioned2024-01-22T17:26:41Z
dc.date.available2024-01-22T17:26:41Z
dc.date.issued2018
dc.description.abstractDifferent families of endogenous lectins use complementary defense strategies against pathogens. They may recognize non-self glycans typically found on pathogens and/or host glycans. The collectin and galectin families are prominent examples of these two lectin categories. Collectins are C-type lectins that contain a carbohydrate recognition domain and a collagen-like domain. Members of this group include surfactant protein A (SP-A) and D (SP-D), secreted by the alveolar epithelium to the alveolar fluid. Lung collectins bind to several microorganisms, which results in pathogen aggregation and/or killing, and enhances phagocytosis of pathogens by alveolar macrophages. Moreover, SP-A and SP-D influence macrophage responses, contributing to resolution of inflammation, and SP-A is essential for tissue-repair functions of macrophages. Galectins also function by interacting directly with pathogens or by modulating the immune system in response to the infection. Direct binding may result in enhanced or impaired infection of target cells, or can have microbicidal effects. Immunomodulatory effects of galectins include recruitment of immune cells to the site of infection, promotion of neutrophil function, and stimulation of the bactericidal activity of infected macrophages. Moreover, intracellular galectins can serve as danger receptors, promoting autophagy of the invading pathogen. This review will focus on the role of collectins and galectins in pathogen clearance and immune response activation in infectious diseases of the respiratory system.
dc.description.departmentDepto. de Bioquímica y Biología Molecular
dc.description.facultyFac. de Ciencias Químicas
dc.description.refereedTRUE
dc.description.sponsorshipMinisterio de Economía y Competitividad (España)
dc.description.sponsorshipInstituto de Salud Carlos III
dc.description.statuspub
dc.identifier.citationCasals C, Campanero-Rhodes MA, García-Fojeda B and Solís D (2018) The Role of Collectins and Galectins in Lung Innate Immune Defense. Front. Immunol. 9:1998. doi: 10.3389/fimmu.2018.01998 Received: 17 June 2018; Accepted: 14 August
dc.identifier.doi10.3389/fimmu.2018.01998
dc.identifier.issn1664-3224
dc.identifier.officialurlhttps://doi.org/10.3389/fimmu.2018.01998
dc.identifier.relatedurlhttps://pubmed.ncbi.nlm.nih.gov/30233589/
dc.identifier.urihttps://hdl.handle.net/20.500.14352/94516
dc.journal.titleFrontiers in Immunology
dc.language.isoeng
dc.page.initial1998
dc.publisherFrontiers
dc.relation.projectIDinfo:eu-repo/grantAgreement/MINECO//SAF2015-65307-R/ES/FACTORES ANTI-INFECCIOSOS DEL PULMON COMO NUEVAS ESTRATEGIAS TERAPEUTICAS FRENTE A INFECCIONES RESPIRATORIAS/
dc.relation.projectIDinfo:eu-repo/grantAgreement/MINECO//BFU2015-70052-R/ES/BUSQUEDA Y DESARROLLO DE NUEVAS APROXIMACIONES PREVENTIVAS Y TERAPEUTICAS FRENTE A LAS INFECCIONES CAUSADAS POR STREPTOCOCCUS PNEUMONIAE/
dc.relation.projectIDCIBERES-CB06/06/0002
dc.relation.projectIDCIBERES-CB06/06/1102
dc.rightsAttribution 4.0 Internationalen
dc.rights.accessRightsopen access
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subject.cdu577.1
dc.subject.keywordAlternatively activated macrophages
dc.subject.keywordAutophagy
dc.subject.keywordInfection
dc.subject.keywordInflammation
dc.subject.keywordLung homeostasis
dc.subject.keywordRespiratory pathogens
dc.subject.keywordSurfactant proteins
dc.subject.keywordTissue repair
dc.subject.ucmBioquímica (Biología)
dc.subject.unesco2412 Inmunología
dc.titleThe Role of Collectins and Galectins in Lung Innate Immune Defense
dc.typejournal article
dc.type.hasVersionVoR
dc.volume.number9
dspace.entity.typePublication
relation.isAuthorOfPublicationd4e23d80-fa5c-4614-bd2d-2c391b596713
relation.isAuthorOfPublication89ed03ac-f011-4290-9a31-7390e12f1724
relation.isAuthorOfPublication.latestForDiscoveryd4e23d80-fa5c-4614-bd2d-2c391b596713

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