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Elevated ILC3s-related Inflammatory Factors May Promote Tendinopathy

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Abstract Background: The prevalence of tendinopathy has risen dramatically over the last few decades and has become a common and serious orthopedic problem in sports injury and elderly populations. Immune cells have been shown to be associated with tendinopathy, with the percentage of Group 3 Innate Lymphoid Cells (ILC3s) having been shown to be upregulated in tendon tissue compared with peripheral blood. Materials and Methods: We used flow cytometry to investigate the percentage of circulating ILC3s in patients with tendinopathy and controls patients; Realtime-PCR was performed to detect the mRNA levels of ILC3s surface markers, CD45, IL-23R, ICOS and ILC3s-related inflammatory factors and transcription factors IL-17A, IL-22 and RORC in tendon samples. Results: Our results showed that the proportion of ILC3s in the peripheral blood circulation of patients with tendinopathy has no significant difference from that of controls by flow cytometry for Lin‑IL-2R+IL-23R + cells; however, the surface marker of ILC3s was upregulated in tendon tissue. In addition, IL-23, a characteristic activating factor of ILC3s, was also upregulated. Relative mRNA expression levels of IL-17A and IL-22 were also upregulated in tendinopathy tendon tissue compared to control patients. Conclusions: These results suggest that ILC3s may be a potential immune factor for tendinopathy.
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Title: Elevated ILC3s-related Inflammatory Factors May Promote Tendinopathy
Description:
Abstract Background: The prevalence of tendinopathy has risen dramatically over the last few decades and has become a common and serious orthopedic problem in sports injury and elderly populations.
Immune cells have been shown to be associated with tendinopathy, with the percentage of Group 3 Innate Lymphoid Cells (ILC3s) having been shown to be upregulated in tendon tissue compared with peripheral blood.
Materials and Methods: We used flow cytometry to investigate the percentage of circulating ILC3s in patients with tendinopathy and controls patients; Realtime-PCR was performed to detect the mRNA levels of ILC3s surface markers, CD45, IL-23R, ICOS and ILC3s-related inflammatory factors and transcription factors IL-17A, IL-22 and RORC in tendon samples.
Results: Our results showed that the proportion of ILC3s in the peripheral blood circulation of patients with tendinopathy has no significant difference from that of controls by flow cytometry for Lin‑IL-2R+IL-23R + cells; however, the surface marker of ILC3s was upregulated in tendon tissue.
In addition, IL-23, a characteristic activating factor of ILC3s, was also upregulated.
Relative mRNA expression levels of IL-17A and IL-22 were also upregulated in tendinopathy tendon tissue compared to control patients.
Conclusions: These results suggest that ILC3s may be a potential immune factor for tendinopathy.

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