gms | German Medical Science

43. Kongress der Deutschen Gesellschaft für Rheumatologie, 29. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie, 25. Wissenschaftliche Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie

02.-05. September 2015, Bremen

γδ T cells as prominent source of IL-17 in SJIA

Meeting Abstract

  • Katrin Lippitz - Universitätsklinikum Münster, Westfälische Wilhelms-Universität, Klinik für Pädiatrische Rheumatologie und Immunologie, Münster
  • Toni Weinhage - Universitätsklinikum Münster, Westfälische Wilhelms-Universität, Klinik für Pädiatrische Rheumatologie und Immunologie, Münster
  • Claas Hinze - Universität Münster, Klinik für Pädiatrische Rheumatologie und Immunologie, Münster
  • Dirk Föll - Universitätsklinikum Münster, Westfälische Wilhelms-Universität, Klinik für Pädiatrische Rheumatologie und Immunologie, Münster
  • Christoph Kessel - Universitätsklinikum Münster, Westfälische Wilhelms-Universität, Klinik für Pädiatrische Rheumatologie und Immunologie, Münster

Deutsche Gesellschaft für Rheumatologie. Deutsche Gesellschaft für Orthopädische Rheumatologie. Gesellschaft für Kinder- und Jugendrheumatologie. 43. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh); 29. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh); 25. wissenschaftliche Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR). Bremen, 02.-05.09.2015. Düsseldorf: German Medical Science GMS Publishing House; 2015. Doc43.02 - KR.47

doi: 10.3205/15dgrh002, urn:nbn:de:0183-15dgrh0024

Veröffentlicht: 1. September 2015

© 2015 Lippitz et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.


Gliederung

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Introduction: Systemic Juvenile Idiopathic Arthritis (SJIA) comprises about 6-20% of all Juvenile Idiopathic Arthritis (JIA) patients and has an incidence of 0.4-0.9 per 100.000 children/year. It presents with arthritis, high spiking fever, erythematous rash, lymphadenopathy, hepatosplenomegaly and serositis. The disease is currently considered to follow a biphasic course in which the initial systemic phase is driven by innate immune mechanisms with IL-1 as key cytokine, while the second more destructive phase appears to be dominated by adaptive immunity and cytokines such as IL-6 or IL-17.

While TH 17 cells are suggested to be enriched in SJIA, the role of γδ T cells as an important IL-17 source at the crossroads between innate and adaptive immunity is poorly defined.

Methods: Whole blood cells from 21 SJIA, 8 Familial Mediterranean Fever (FMF; as systemic inflammation control group), and 13 pediatric health control samples were left untreated or were stimulated with phorbol 12-myristate 13-acetate (PMA) and ionomycin in presence of protein transport inhibitors (brefeldin A and monensin). Unstimulated as well as stimulated cells were stained for expression of CD3, CD4, TCRγδ, IL-17, IL-22 and INFγ and analyzed by flow cytometry.

Results: Although significantly increased numbers of CD3+CD4+ T cells were found in SJIA as well as in FMF patient samples compared to healthy controls, cells expressing TCRγδ are significantly under-represented in particularly SJIA patients’ whole blood. Patients’ follow-up samples suggest γδ T cell levels to be reduced in active disease and to re-establish during remission. Yet, although fewer in number, SJIA γδ T cells express high levels of particularly IL-17 compared to healthy controls. γδ T cellular IL-17 production tends to be even further increased in active SJIA, while levels in quiescent disease still remain significantly elevated.

Conclusion: Albeit the overall frequency of γδ T cells is particularly reduced in SJIA, these cells pose a prominent source for IL-17 in active but also quiescent disease. As the reduction in γδ T cell counts appears to negatively correlate with disease activity, monitoring these cell counts in peripheral blood may serve as marker in following patients’ therapy and eventually supports predicting disease flares.