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A Positive Feedback Loop Between Th17 Cells and Dendritic Cells in Patients with Endplate Inflammation. | LitMetric

AI Article Synopsis

  • Endplate inflammation is a challenging condition to treat, and previous research indicated an increase in Th17 cells among affected patients, suggesting a role in the disease's pathology.
  • The study analyzed Th17 cells from both patients and healthy individuals and found that Th17 cells enhanced the maturation and activation of specific dendritic cells (DCs) even without external triggers, with a stronger effect observed in cells from patients.
  • The findings suggest that Th17 cells from patients can create a feedback loop that boosts IL-17 production by naive CD4+ T cells, highlighting their significant role in driving inflammation in endplate disease.

Article Abstract

Background: Endplate inflammation remains a difficult disease to treat, in part due to its unclear pathology. Previous experiments showed that patients with idiopathic inflammation presented a systemic upregulation of Th17 cells. Here, we investigated how this change might affect the inflammatory environment in endplate inflammation.

Methods: Peripheral blood was obtained from patients and healthy controls, and Th17 cells were examined.

Results: Th17 cells significantly increased the differentiation of CD11c+ and DC-SIGN+ dendritic cells (DCs) from circulating monocytes in the absence of exogenous stimulation as well as in the presence of LPS stimulation. Th17 cells also increased CD80 and CD86 expression by DCs. Importantly, although Th17 cells from both healthy controls and patients with endplate inflammation could induce CD11c, DC-SIGN, CD80, and CD86 expression, Th17 cells from patients with endplate inflammation showed significantly more potent capacity. Both contact-dependent and IL-17-dependent mechanisms were employed by Th17 cells, since blocking cell-to-cell contact significantly inhibited Th17-mediated differentiation of CD11c+ DCs, and neutralization of IL-17 reduced the expression of CD80 and CD86. Strikingly, DCs following incubation with Th17 cells, but not the DCs derived directly from monocytes without Th17 cells, could significantly promote the expression of IL-17 from naive CD4+ T cells.

Conclusions: These results demonstrated that Th17 cells from patients with endplate inflammation could potently induce the differentiation and activation of DCs that preferentially promoted IL-17 response in a positive feedback loop.

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Source
http://dx.doi.org/10.1080/08820139.2018.1496097DOI Listing

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