Your browser doesn't support javascript.
loading
The TAM family receptor tyrosine kinase TYRO3 is a negative regulator of type 2 immunity.
Chan, Pamela Y; Carrera Silva, Eugenio A; De Kouchkovsky, Dimitri; Joannas, Leonel D; Hao, Liming; Hu, Donglei; Huntsman, Scott; Eng, Celeste; Licona-Limón, Paula; Weinstein, Jason S; Herbert, De'Broski R; Craft, Joseph E; Flavell, Richard A; Repetto, Silvia; Correale, Jorge; Burchard, Esteban G; Torgerson, Dara G; Ghosh, Sourav; Rothlin, Carla V.
Afiliação
  • Chan PY; Department of Immunobiology, School of Medicine, Yale University, New Haven, CT 06520, USA.
  • Carrera Silva EA; Department of Immunobiology, School of Medicine, Yale University, New Haven, CT 06520, USA. Laboratorio de Trombosis Experimental, Instituto de Medicina Experimental, Academia Nacional de Medicina-CONICET, Buenos Aires, 1425, Argentina.
  • De Kouchkovsky D; Department of Immunobiology, School of Medicine, Yale University, New Haven, CT 06520, USA.
  • Joannas LD; Department of Immunobiology, School of Medicine, Yale University, New Haven, CT 06520, USA.
  • Hao L; Department of Pathology, School of Medicine, Yale University, New Haven, CT 06520, USA.
  • Hu D; Department of Medicine, University of California San Francisco, CA 94158, USA.
  • Huntsman S; Department of Medicine, University of California San Francisco, CA 94158, USA.
  • Eng C; Department of Medicine, University of California San Francisco, CA 94158, USA.
  • Licona-Limón P; Department of Immunobiology, School of Medicine, Yale University, New Haven, CT 06520, USA.
  • Weinstein JS; Department of Immunobiology, School of Medicine, Yale University, New Haven, CT 06520, USA.
  • Herbert DR; Department of Experimental Medicine, University of California San Francisco, CA 94158, USA.
  • Craft JE; Department of Immunobiology, School of Medicine, Yale University, New Haven, CT 06520, USA. Department of Internal Medicine (Rheumatology), School of Medicine, Yale University, New Haven, CT 06520, USA.
  • Flavell RA; Department of Immunobiology, School of Medicine, Yale University, New Haven, CT 06520, USA. Howard Hughes Medical Institute, School of Medicine, Yale University, New Haven, CT 06520, USA.
  • Repetto S; Instituto de Investigaciones en Microbiología y Parasitología Médica, University of Buenos Aires-CONICET, Buenos Aires, 1121, Argentina. Hospital de Clinicas Jose de San Martin, University of Buenos Aires, 1120, Argentina.
  • Correale J; Center for Research on Neuroimmunological Diseases, Raúl Carrea Institute for Neurological Research (FLENI), Buenos Aires 1428, Argentina.
  • Burchard EG; Department of Medicine, University of California San Francisco, CA 94158, USA. Department of Bioengineering, School of Pharmacy, University of California San Francisco, CA 94158, USA.
  • Torgerson DG; Department of Medicine, University of California San Francisco, CA 94158, USA.
  • Ghosh S; Department of Neurology, School of Medicine, Yale University, New Haven, CT 06520, USA.
  • Rothlin CV; Department of Immunobiology, School of Medicine, Yale University, New Haven, CT 06520, USA. carla.rothlin@yale.edu.
Science ; 352(6281): 99-103, 2016 Apr 01.
Article em En | MEDLINE | ID: mdl-27034374
ABSTRACT
Host responses against metazoan parasites or an array of environmental substances elicit type 2 immunity. Despite its protective function, type 2 immunity also drives allergic diseases. The mechanisms that regulate the magnitude of the type 2 response remain largely unknown. Here, we show that genetic ablation of a receptor tyrosine kinase encoded byTyro3in mice or the functional neutralization of its ortholog in human dendritic cells resulted in enhanced type 2 immunity. Furthermore, the TYRO3 agonist PROS1 was induced in T cells by the quintessential type 2 cytokine, interleukin-4. T cell-specificPros1knockouts phenocopied the loss ofTyro3 Thus, a PROS1-mediated feedback from adaptive immunity engages a rheostat, TYRO3, on innate immune cells to limit the intensity of type 2 responses.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Asma / Receptores Proteína Tirosina Quinases / Imunidade Adaptativa / Interações Hospedeiro-Parasita / Imunidade Inata Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Ano de publicação: 2016 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Asma / Receptores Proteína Tirosina Quinases / Imunidade Adaptativa / Interações Hospedeiro-Parasita / Imunidade Inata Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Ano de publicação: 2016 Tipo de documento: Article