Mostrar el registro sencillo del ítem
dc.contributor.author
Carrera Silva, Eugenio Antonio
dc.contributor.author
Chan, Pamela Y.
dc.contributor.author
Joannas, Leonel
dc.contributor.author
Errasti, Andrea Emilse
dc.contributor.author
Gagliani, Nicola
dc.contributor.author
Bosurgi, Lidia
dc.contributor.author
Jabbour, Maurice
dc.contributor.author
Perry, Anthony
dc.contributor.author
Smith Chakmakova, Faye
dc.contributor.author
Mucida, Daniel
dc.contributor.author
Cheroutre, Hilde
dc.contributor.author
Burstyn Cohen, Tal
dc.contributor.author
Leighton, Jonathan A.
dc.contributor.author
Lemke, Greg
dc.contributor.author
Ghosh, Sourav
dc.contributor.author
Rothlin, Carla V.
dc.date.available
2015-08-25T14:34:37Z
dc.date.issued
2013-07-25
dc.identifier.citation
Carrera Silva, Eugenio Antonio; Chan, Pamela Y.; Joannas, Leonel; Errasti, Andrea Emilse; Gagliani, Nicola; et al.; T Cell-Derived Protein S Engages TAM Receptor Signaling in Dendritic Cells to Control the Magnitude of the Immune Response; Elsevier; Immunity; 39; 1; 25-7-2013; 160-170
dc.identifier.issn
1074-7613
dc.identifier.uri
http://hdl.handle.net/11336/1807
dc.description.abstract
Dendritic cell (DC) activation is essential for the induction of immune defense against pathogens, yet needs to be tightly controlled to avoid chronic inflammation and exaggerated immune responses. Here, we identify a mechanism of immune homeostasis by which adaptive immunity, once triggered, tempers DC activation and prevents overreactive immune responses. T cells, once activated, produced Protein S (Pros1) that signaled through TAM receptor tyrosine kinases in DCs to limit the magnitude of DC activation. Genetic ablation of Pros1 in mouse T cells led to increased expression of costimulatory molecules and cytokines in DCs and enhanced immune responses to T cell-dependent antigens, as well as increased colitis. Additionally, PROS1 was expressed in activated human T cells, and its ability to regulate DC activation was conserved. Our results identify a heretofore unrecognized, homeostatic negative feedback mechanism at the interface of adaptive and innate immunity that maintains the physiological magnitude of the immune response.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Elsevier
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
T Cells
dc.subject
Pros1
dc.subject
Dendritic Cell Activation
dc.subject.classification
Inmunología
dc.subject.classification
Medicina Básica
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
T Cell-Derived Protein S Engages TAM Receptor Signaling in Dendritic Cells to Control the Magnitude of the Immune Response
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2016-03-30 10:35:44.97925-03
dc.journal.volume
39
dc.journal.number
1
dc.journal.pagination
160-170
dc.journal.pais
Países Bajos
dc.journal.ciudad
Amsterdam
dc.description.fil
Fil: Carrera Silva, Eugenio Antonio. University of Yale. School of Medicine; Estados Unidos de América; Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental; Argentina;
dc.description.fil
Fil: Chan, Pamela Y.. University of Yale. School of Medicine; Estados Unidos de América;
dc.description.fil
Fil: Joannas, Leonel. University of Yale. School of Medicine; Estados Unidos de América;
dc.description.fil
Fil: Errasti, Andrea Emilse. Universidad de Buenos Aires. Facultad de Medicina. Cátedra de Farmacología; Argentina; University of Yale. School of Medicine; Estados Unidos de América; Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina;
dc.description.fil
Fil: Gagliani, Nicola. University of Yale. School of Medicine; Estados Unidos de América;
dc.description.fil
Fil: Bosurgi, Lidia. University of Yale. School of Medicine; Estados Unidos de América;
dc.description.fil
Fil: Jabbour, Maurice. University Of Arizona; Estados Unidos de América;
dc.description.fil
Fil: Perry, Anthony. Banner MD Anderson Cancer Center; Estados Unidos de América;
dc.description.fil
Fil: Smith Chakmakova, Faye. Saint Joseph’s Hospital and Medical Center; Estados Unidos de América;
dc.description.fil
Fil: Mucida, Daniel. La Jolla Institute for Allergy and Immunology; Estados Unidos de América;
dc.description.fil
Fil: Cheroutre, Hilde. La Jolla Institute for Allergy and Immunology; Estados Unidos de América;
dc.description.fil
Fil: Burstyn Cohen, Tal. Salk Institute for Biological Studies; Estados Unidos de América;
dc.description.fil
Fil: Leighton, Jonathan A.. Mayo Clinic Arizona; Estados Unidos de América;
dc.description.fil
Fil: Lemke, Greg. Salk Institute for Biological Studies; Estados Unidos de América;
dc.description.fil
Fil: Ghosh, Sourav. University Of Arizona; Estados Unidos de América;
dc.description.fil
Fil: Rothlin, Carla V.. University of Yale. School of Medicine; Estados Unidos de América;
dc.journal.title
Immunity
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4017237/
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/doi:10.1016/j.immuni.2013.06.010
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S107476131300277X
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://www.cell.com/immunity/abstract/S1074-7613(13)00277-X
Archivos asociados