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Endothelial Cell-Derived Soluble CD200 Determines the Ability of Immune Cells to Cross the Blood-Brain Barrier.
Pujol, Myriam; Paskevicius, Tautvydas; Robinson, Alison; Dhillon, Simran; Eggleton, Paul; Ferecskó, Alex S; Gutowski, Nick; Holley, Janet; Smallwood, Miranda; Newcombe, Jia; Agellon, Luis B; Michalak, Marek.
Afiliación
  • Pujol M; Department of Biochemistry, University of Alberta, Edmonton, AB T6G 2H7, Canada.
  • Paskevicius T; Department of Biochemistry, University of Alberta, Edmonton, AB T6G 2H7, Canada.
  • Robinson A; Department of Biochemistry, University of Alberta, Edmonton, AB T6G 2H7, Canada.
  • Dhillon S; Department of Biochemistry, University of Alberta, Edmonton, AB T6G 2H7, Canada.
  • Eggleton P; Revolo Biotherapeutics, Gaithersburg, MD 20878, USA.
  • Ferecskó AS; University of Exeter Medical School, University of Exeter, Exeter EX1 2HZ, UK.
  • Gutowski N; University of Exeter Medical School, University of Exeter, Exeter EX1 2HZ, UK.
  • Holley J; University of Exeter Medical School, University of Exeter, Exeter EX1 2HZ, UK.
  • Smallwood M; University of Exeter Medical School, University of Exeter, Exeter EX1 2HZ, UK.
  • Newcombe J; University of Exeter Medical School, University of Exeter, Exeter EX1 2HZ, UK.
  • Agellon LB; NeuroResource, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, University College London, London WC1E 6BT, UK.
  • Michalak M; School of Human Nutrition, McGill University, Sainte Anne de Bellevue, QC H9X 3V9, Canada.
Int J Mol Sci ; 25(17)2024 Aug 27.
Article en En | MEDLINE | ID: mdl-39273210
ABSTRACT
The infiltration of immune cells into the central nervous system mediates the development of autoimmune neuroinflammatory diseases. We previously showed that the loss of either Fabp5 or calnexin causes resistance to the induction of experimental autoimmune encephalomyelitis (EAE) in mice, an animal model of multiple sclerosis (MS). Here we show that brain endothelial cells lacking either Fabp5 or calnexin have an increased abundance of cell surface CD200 and soluble CD200 (sCD200) as well as decreased T-cell adhesion. In a tissue culture model of the blood-brain barrier, antagonizing the interaction of CD200 and sCD200 with T-cell CD200 receptor (CD200R1) via anti-CD200 blocking antibodies or the RNAi-mediated inhibition of CD200 production by endothelial cells increased T-cell adhesion and transmigration across monolayers of endothelial cells. Our findings demonstrate that sCD200 produced by brain endothelial cells regulates immune cell trafficking through the blood-brain barrier and is primarily responsible for preventing activated T-cells from entering the brain.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Barrera Hematoencefálica / Linfocitos T / Antígenos CD / Adhesión Celular / Células Endoteliales Límite: Animals / Humans Idioma: En Revista: Int J Mol Sci Año: 2024 Tipo del documento: Article País de afiliación: Canadá Pais de publicación: Suiza
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Barrera Hematoencefálica / Linfocitos T / Antígenos CD / Adhesión Celular / Células Endoteliales Límite: Animals / Humans Idioma: En Revista: Int J Mol Sci Año: 2024 Tipo del documento: Article País de afiliación: Canadá Pais de publicación: Suiza