gms | German Medical Science

47. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh), 33. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh), 29. Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR)

04.09. - 07.09.2019, Dresden

Expression of inhibitory receptor PIR-B on peripheral T cells in arthritis mouse model

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  • Kathrin Rothe - Universitätsklinikum Leipzig, Klinik und Poliklinik für Gastroenterologie und Rheumatologie, Sektion Rheumatologie, Leipzig
  • Dagmar Quandt - Universitätsklinikum Leipzig, Klinik und Poliklinik für Gastroenterologie und Rheumatologie, Sektion Rheumatologie, Leipzig
  • Gabriele Köhler - Institute of Pathology, Fulda
  • Ulf Wagner - Universitätsklinikum Leipzig, Klinik und Poliklinik für Gastroenterologie und Rheumatologie, Sektion Rheumatologie, Leipzig

Deutsche Gesellschaft für Rheumatologie. Deutsche Gesellschaft für Orthopädische Rheumatologie. Gesellschaft für Kinder- und Jugendrheumatologie. 47. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh), 33. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh), 29. Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR). Dresden, 04.-07.09.2019. Düsseldorf: German Medical Science GMS Publishing House; 2019. DocRA.40

doi: 10.3205/19dgrh214, urn:nbn:de:0183-19dgrh2148

Published: October 8, 2019

© 2019 Rothe et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.


Outline

Text

Background: T cells in rheumatoid arthritis are dysregulated with a pro-inflammatory cytokine profile. We previously identified a subset of effector-memory CD8+ and CD4+ T cell which are characterized by the expression of inhibitory receptor LIR-1 and an increased cytolytic potential. To elucidate the in vivo role of LIR-1+ T cells, we investigated the expression of its orthologue PIR-B in SKG and collagen-induced arthritis (CIA) mouse model.

Methods: Surface expression of PIR-B on CD8+ and CD4+ T cells from spleen, lymph nodes and peripheral blood was analyzed using flow cytometry and RT-PCR. For functional studies, isolated T cells were stimulated via PMA/ionomycin and production of IL-17 and IFN-γ was analyzed immediately. Arthritis score was analyzed after arthritis induction by evaluation of paw swelling. In a blinded fashion, histological analysis of synovial sections was performed after H&E staining by evaluation of inflammation and cell infiltration.

Results: SKG mice show increased frequencies of splenic PIR-B+ T cells in comparison to age-matched wildtype background mice. Additionally, arthritis induction supports expansion of PIR-B+ T cells. Stimulation with PMA/ionomycin revealed that PIR-B+ T cells are mainly pro-inflammatory by a large production of IFN-γ and contain a subset of IL-17 producer. In contrast to cytokine production, frequencies of PIR-B+ T cells were negatively associated with arthritis or histological score.

Conclusion: We are the first, who showed expression of inhibitory receptor PIR-B on peripheral T cells in SKG and CIA mouse model. PIR-B+ T cells seem to take part in arthritis pathogenesis, since the number negatively correlates with arthritis disease severity.