IL-17 and IFN-γ producing NK and γδ-T cells are preferentially expanded in synovial fluid of patients with reactive arthritis and undifferentiated spondyloarthritis

Chowdhury, Abhra Chandra; Chaurasia, Smriti; Mishra, Sudhish; Aggarwal, Amita; Misra, Ramnath

doi:10.1016/j.clim.2017.03.016

Cited by 42 publications

(22 citation statements)

References 29 publications

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“…Subsequently, the frequency of IL-17A expressing γδ T cells was reported to be increased in the peripheral blood of patients with PsA, AS, reactive arthritis and enthesisrelated JIA compared with healthy controls [168][169][170] . IL-17A+ γδ T cells are also enriched in the synovial fluid compared with the peripheral blood of patients with PsA, reactive arthritis or undifferentiated SpA 170,171 .…”

Section: γδ T Cells  T Cells Are a Subset Of T Cells That Combine Tmentioning

confidence: 99%

IL-17 in the immunopathogenesis of spondyloarthritis

et al. 2018

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Spondyloarthritis (SpA) is a term that refers to a group of inflammatory diseases that includes psoriatic arthritis, axial SpA and nonradiographic axial SpA, reactive arthritis, enteropathic arthritis and undifferentiated SpA. The disease subtypes share clinical and immunological features, including joint inflammation (peripheral and axial skeleton); skin, gut and eye manifestations; and the absence of diagnostic autoantibodies (seronegative). The diseases also share genetic factors. The aetiology of SpA is still the subject of research by many groups worldwide. Evidence from genetic, experimental and clinical studies has accumulated to indicate a clear role for the IL-17 pathway in the pathogenesis of SpA. The IL-17 family consists of IL-17A, IL-17B, IL-17C, IL-17D, IL-17E and IL-17F, of which IL-17A is the best studied. IL-17A is a pro-inflammatory cytokine that also has the capacity to promote angiogenesis and osteoclastogenesis. Of the six family members, IL-17A has the strongest homology with IL-17F. In this Review, we discuss how IL-17A and IL-17F and their cellular sources might contribute to the immunopathology of SpA.

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Section: γδ T Cells  T Cells Are a Subset Of T Cells That Combine Tmentioning

confidence: 99%

IL-17 in the immunopathogenesis of spondyloarthritis

et al. 2018

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“…Intraepithelial γδT cells can also limit transepithelial pathogen invasion and contribute to immune protection in mucosal tissues (19). On the other hand, γδT cells can enhance the pathogenesis of inflammatory diseases, such as psoriasis-like dermatitis and spondyloarthritis (20,21).…”

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confidence: 99%

Mutual interplay between IL-17–producing γδT cells and microbiota orchestrates oral mucosal homeostasis

Wilharm

Tabib

Nassar

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

138

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γδT cells are a major component of epithelial tissues and play a role in tissue homeostasis and host defense. γδT cells also reside in the gingiva, an oral tissue covered with specialized epithelium that continuously monitors the challenging dental biofilm. Whereas most research on intraepithelial γδT cells focuses on the skin and intestine epithelia, our knowledge on these cells in the gingiva is still incomplete. In this study, we demonstrate that even though the gingiva develops after birth, the majority of gingival γδT cells are fetal thymus-derived Vγ6+ cells, and to a lesser extent Vγ1+ and Vγ4+ cells. Furthermore, we show that γδT cells are motile and locate preferentially in the epithelium adjacent to the biofilm. Vγ6+ cells represent the major source of IL-17–producing cells in the gingiva. Chimeric mice and parabiosis experiments indicated that the main fraction of gingival γδT cells is radioresistant and tissue-resident, persisting locally independent of circulating γδT cells. Notably, gingival γδT cell homeostasis is regulated by the microbiota as the ratio of Vγ6+ and Vγ4+ cells was reversed in germ-free mice, and their activation state was decreased. As a consequence, conditional ablation of γδT cells results in elevated gingival inflammation and subsequent alterations of oral microbial diversity. Taken together, these findings suggest that oral mucosal homeostasis is shaped by reciprocal interplays between γδT cells and local microbiota.

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“…Strikingly, this phenotype was absent in rheumatoid arthritis patients ( 54 ), suggesting specific involvement of IL-17-producing γδ T cells in SpA pathogenesis rather than in arthritic inflammation in general. Along the same line, the analysis of tissue samples from enthesitis-related arthritis ( 55 ), reactive arthritis or undifferentiated SpA ( 56 ) as well as juvenile idiopathic arthritis (JIA) patients ( 57 ) revealed an increase in blood and synovial fluid IL-17-producing γδ T cells. Notably, such increased numbers of IL-17-producing γδ T cells might be driven by a defined arthritic cytokine environment ( 57 ).…”

Section: Introductionmentioning

confidence: 93%

Whodunit? The Contribution of Interleukin (IL)-17/IL-22-Producing γδ T Cells, αβ T Cells, and Innate Lymphoid Cells to the Pathogenesis of Spondyloarthritis

Reinhardt

Prinz

2018

Front. Immunol.

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γδ T cells, αβ T cells, and innate lymphoid cells (ILCs) are capable of producing interleukin (IL)-17A, IL-17F, and IL-22. Among these three families of lymphocytes, it is emerging that γδ T cells are, at least in rodents, the main source of these key pro-inflammatory cytokines. γδ T cells were implicated in multiple inflammatory and autoimmune diseases, including psoriasis, experimental autoimmune encephalomyelitis and uveitis, colitis, and rheumatoid arthritis. Recent findings pointed toward a central role of γδ T cells in the pathogenesis of spondyloarthritis (SpA), a group of inflammatory rheumatic diseases affecting the axial skeleton. SpA primarily manifests as inflammation and new bone formation at the entheses, which are connecting tendons or ligaments with bone. In SpA patients, joint inflammation is frequently accompanied by extra-articular manifestations, such as inflammatory bowel disease or psoriasis. In humans, genome-wide association studies could link the IL-23/IL-17 cytokine axis to SpA. Accordingly, antibodies targeting IL-23/IL-17 for SpA treatment already showed promising results in clinical studies. However, the contribution of IL-17-producing γδ T cells to SpA pathogenesis is certainly not an open-and-shut case. Indeed, the cell types that are chiefly involved in local inflammation in human SpA still remain largely unclear. Some studies focusing on blood or synovium from SpA patients reported augmented IL-17-producing and IL-23 receptor-expressing γδ T cells, but other cell types might contribute as well. Here, we summarize the current understanding of how γδ T cells, αβ T cells, and ILCs contribute to the pathogenesis of human and experimental SpA.

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IL-17 and IFN-γ producing NK and γδ-T cells are preferentially expanded in synovial fluid of patients with reactive arthritis and undifferentiated spondyloarthritis

Cited by 42 publications

References 29 publications

IL-17 in the immunopathogenesis of spondyloarthritis

IL-17 in the immunopathogenesis of spondyloarthritis

Mutual interplay between IL-17–producing γδT cells and microbiota orchestrates oral mucosal homeostasis

Whodunit? The Contribution of Interleukin (IL)-17/IL-22-Producing γδ T Cells, αβ T Cells, and Innate Lymphoid Cells to the Pathogenesis of Spondyloarthritis

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