γδTCR regulates production of interleukin-27 by neutrophils and attenuates inflammatory arthritis

Laura Bouchareychas, Eva M. Grössinger, Mincheol Kang, Iannis Adamopoulos

Research output: Contribution to journalArticle

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Abstract

γδ T cells have been implicated in inflammatory diseases as an important link between the innate and adaptive immune responses, however, their role in inflammatory arthritis remain unclear. To define the contribution of γδ T cells in the pathogenesis of inflammatory arthritis, we performed gene transfer of IL-23 in B10.RIII mice to establish joint inflammation in the presence or absence of γδ T cells. We demonstrated that γδ T cell blockade has a protective effect on arthritis incidence and severity by preventing neutrophil accumulation in the blood, spleen and bone marrow as well as by reducing neutrophil infiltration into the joints. Furthermore, our data demonstrate that absence of γδ T cells was associated with an increase of IL-27 levels produced by neutrophils and dendritic cells, and systemic IL-27 expression also prevents IL-23-induced inflammatory arthritis and limits neutrophil expansion. Collectively our findings reveal an immunomodulatory effect of γδ T cells on neutrophils associated with IL-27 synthesis and secretion and indicate a novel link between IL-27 and the modulation of γδ T cells and neutrophils that can be targeted in the treatment of inflammatory arthritis.

Original languageEnglish (US)
Article number7590
JournalScientific Reports
Volume8
Issue number1
DOIs
StatePublished - Dec 1 2018

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Interleukin-27
Arthritis
Neutrophils
T-Lymphocytes
Interleukin-23
Joints
Neutrophil Infiltration
Adaptive Immunity
Innate Immunity
Dendritic Cells
Spleen
Bone Marrow
Inflammation
Incidence

ASJC Scopus subject areas

  • General

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γδTCR regulates production of interleukin-27 by neutrophils and attenuates inflammatory arthritis. / Bouchareychas, Laura; Grössinger, Eva M.; Kang, Mincheol; Adamopoulos, Iannis.

In: Scientific Reports, Vol. 8, No. 1, 7590, 01.12.2018.

Research output: Contribution to journalArticle

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