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Survivin co-ordinates formation of follicular T-cells acting in synergy with Bcl-6

Journal article
Authors Karin Andersson
Mikael Brisslert
Nicola Cavallini
Mattias Svensson
Amanda Welin
Malin Erlandsson
M. J. Ciesielski
Gergely Katona
Maria Bokarewa
Published in Oncotarget
Volume 6
Issue 24
Pages 20043-20057
ISSN 1949-2553
Publication year 2015
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Department of Chemistry and Molecular Biology
Pages 20043-20057
Language en
Links dx.doi.org/10.18632/oncotarget.4994
Keywords Immunology Section, survivin, Bcl6, T-cells, autoimmunity, arthritis, EARLY RHEUMATOID-ARTHRITIS, GERMINAL-CENTER B, ALLEVIATES EXPERIMENTAL, ARTHRITIS, COLLAGEN-INDUCED ARTHRITIS, PHOSPHORYLATED HISTONE H3, CXC, CHEMOKINE RECEPTOR-5, HELPER TFH CELLS, LYMPHOCYTE DIFFERENTIATION, CITRULLINATED PEPTIDES, DISEASE-ACTIVITY, Oncology, Cell Biology
Subject categories Rheumatology and Autoimmunity, Immunobiology

Abstract

Follicular T helper (Tfh) cells are recognized by the expression of CXCR5 and the transcriptional regulator Bcl-6. Tfh cells control B cell maturation and antibody production, and if deregulated, may lead to autoimmunity. Here, we study the role of the proto-oncogene survivin in the formation of Tfh cells. We show that blood Tfh cells of patients with the autoimmune condition rheumatoid arthritis, have intracellular expression of survivin. Survivin was co-localized with Bcl-6 in the nuclei of CXCR5(+)CD4 lymphocytes and was immunoprecipitated with the Bcl-6 responsive element of the target genes. Inhibition of survivin in arthritic mice led to the reduction of CXCR5(+) Tfh cells and to low production of autoantibodies. Exposure to survivin activated STAT3 and induced enrichment of PD-1(+)Bcl-6(+) subset within Tfh cells. Collectively, our study demonstrates that survivin belongs to the Tfh cell phenotype and ensures their optimal function by regulating transcriptional activity of Bcl-6.

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