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Originally published online as doi:10.1189/jlb.0507287 on October 15, 2007

Published online before print October 15, 2007
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(Journal of Leukocyte Biology. 2008;83:149-155.)
© 2008 by Society for Leukocyte Biology

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

Simona Mera, Mattias Magnusson, Andrej Tarkowski and Maria Bokarewa1

Department of Rheumatology and Inflammation Research, Sahlgrenska University Hospital, Göteborg, Sweden

1 Correspondence: Department of Rheumatology and Inflammation Research, Guldhedsgatan 10, S-413 46 Göteborg, Sweden. E-mail: maria.bokarewa{at}rheuma.gu.se

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 β-integrins and their ligand ICAM-1. Survivin-induced expression of {alpha}-chains of β2-integrins is regulated by p38 MAPK and PI-3K but not by the NF-{kappa}B 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.

Key Words: β2-integrins • survivin • p38 • inflammation • rheumatoid arthritis




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