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Göteborgs universitets publikationer

Extracellular survivin up-regulates adhesion molecules on the surface of leukocytes changing their reactivity pattern.

Författare och institution:
Simona Mera (-); Mattias Magnusson (Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning); Andrej Tarkowski (Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning); Maria Bokarewa (Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning)
Publicerad i:
Journal of leukocyte biology, 83 ( 1 ) s. 149-55
Artikel, refereegranskad vetenskaplig
Sammanfattning (abstract):
Rheumatoid arthritis (RA) is an autoimmune disease with joints as a principal target of inflammation. We have shown recently that the extracellular expression of the antiapoptotic protein survivin is associated with a destructive course of RA. Here, we address the potential impact of extracellular survivin on peripheral blood leukocytes (PBL). The binding of survivin to the surface of human PBL as well as the expression of adhesion molecules were assessed by FACS. The expression of adhesion molecules on leukocytes as a function of circulating survivin was analyzed in blood of 24 patients with RA and compared with eight healthy individuals. We show that extracellular survivin expresses immunomodulatory properties. It binds to the surface of the majority of granulocytes and a significant part of lymphocytes and monocytes inducing the activation of alpha-chains of beta-integrins and their ligand ICAM-1. Survivin-induced expression of alpha-chains of beta 2-integrins is regulated by p38 MAPK and PI-3K but not by the NF-kappaB signaling pathway. Clinical relevance of our findings is supported by the in vivo association of high circulating survivin levels with an increased expression of CD11c on monocytes and granulocytes in RA patients. The results of our study demonstrate that extracellular survivin affects the phenotype of leukocytes having a possible impact on homing of inflammatory cells during arthritis.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
1-Phosphatidylinositol 3-Kinase, immunology, Antigens, CD18, biosynthesis, drug effects, immunology, Arthritis, Rheumatoid, blood, diagnosis, immunology, Cell Adhesion Molecules, drug effects, immunology, Extracellular Space, metabolism, Humans, Leukocytes, drug effects, immunology, Microtubule-Associated Proteins, biosynthesis, immunology, pharmacology, Neoplasm Proteins, biosynthesis, immunology, pharmacology, Recombinant Proteins, biosynthesis, immunology, pharmacology, Signal Transduction, immunology, Up-Regulation, drug effects, immunology, p38 Mitogen-Activated Protein Kinases, immunology
Postens nummer:
Posten skapad:
2009-01-07 13:18
Posten ändrad:
2011-01-20 10:00

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