期刊
MODERN RHEUMATOLOGY
卷 24, 期 3, 页码 434-442出版社
TAYLOR & FRANCIS LTD
DOI: 10.3109/14397595.2013.844309
关键词
Autoimmunity; CD1d; Rheumatoid arthritis; alpha GalCer; NKT cells; V alpha 24(+) cells
类别
资金
- Arthritis Research UK [P0571]
- Wellcome Leave Clinical Fellowship [GR061125]
- Internal Rheumatology Studentship from the University of Liverpool
- Medical Research Council [G1001539, MR/K026453/1] Funding Source: researchfish
- MRC [MR/K026453/1, G1001539] Funding Source: UKRI
Objectives. While numerical and functional defects of invariant NKT cells have been demonstrated in rheumatoid arthritis (RA), the detailed characterization of proliferative and secretory responses following CD1d-mediated presentation is lacking; the presence of non-invariant populations has never been assessed in human autoimmunity. We have evaluated both invariant and non-invariant populations in the blood and synovial fluid from patients to assess feasibility of NKT cell-directed manipulations in RA. Methods. NKT cell populations were quantified by anti-CD4/anti-V alpha 24 staining and/or CD1d tetramers. Proliferation was measured in cultures of mononuclear cells following stimulations with a GalCer and cytokine secretion determined by multi-bead assay. Results. We have confirmed a proliferative defect of iNKT cells in both peripheral blood and synovial fluid from RA patients, but no changes in baseline frequencies. Moreover, we have detected an enlargement of non-invariant cell pool in synovial fluid samples. In addition, we noted an evident Th2 shift following exposure to a GalCer and pronounced IL-6 secretion. Conclusions. While RA patients suffer from defective proliferative responses of invariant NKT cells, non-invariant cells accumulate at the site of inflammation. While stimulation with a GalCer results in reduced TNF-alpha and increased suppressive IL-10, abundantly produced IL-6 could potentially contribute to the induction of Th17 cells in the joints.
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