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Schauer, M.* ; Kleinwort, K.J.H.* ; Degroote, R.L.* ; Wiedemann, C.* ; Kremmer, E. ; Hauck, S.M. ; Deeg, C.A.*

Interaction of septin 7 and DOCK8 in equine lymphocytes reveals novel insights into signaling pathways associated with autoimmunity.

Sci. Rep. 8:12332 (2018)

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The GTP-binding protein septin 7 is involved in various cellular processes, including cytoskeleton organization, migration and the regulation of cell shape. Septin 7 function in lymphocytes, however, is poorly characterized. Since the intracellular signaling role of septin 7 is dependent on its interaction network, interaction proteomics was applied to attain novel knowledge about septin 7 function in hematopoietic cells. Our previous finding of decreased septin 7 expression in blood-derived lymphocytes in ERU, a spontaneous animal model for autoimmune uveitis in man, extended the role of septin 7 to a potential key player in autoimmunity. Here, we revealed novel insights into septin 7 function by identification of DOCK8 as an interaction partner in primary blood-derived lymphocytes. Since DOCK8 is associated with important immune functions, our finding of significantly decreased DOCK8 expression and altered DOCK8 interaction network in ERU might explain changes in immune response and shows the contribution of DOCK8 in pathomechanisms of spontaneous autoimmune diseases. Moreover, our analyses revealed insights in DOCK8 function, by identifying the signal transducer ILK as a DOCK8 interactor in lymphocytes. Our finding of the enhanced enrichment of ILK in ERU cases indicates a deviant influence of DOCK8 on inter-and intracellular signaling in autoimmune disease.

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Publication type Article: Journal article

Document type Scientific Article

Corresponding Author

Keywords Integrin-linked Kinase; Recurrent Uveitis; Mammalian Septins; T-lymphocytes; Talin 1; Dedicator; Cytoskeleton; Deficiency; Survival; Horses

ISSN (print) / ISBN 2045-2322

e-ISSN 2045-2322

Journal Scientific Reports

Quellenangaben Volume: 8, Issue: 1, Article Number: 12332

Publisher Nature Publishing Group

Publishing Place London

Non-patent literature Publications

Reviewing status Peer reviewed

Institute(s) CF Monoclonal Antibodies (CF-MAB)
CF Metabolomics & Proteomics (CF-MPC)