The characterization and clinical significance of PI3K/ Akt signaling pathway activation in the peripheral T cells of pediatric patients with atopic dermatitis

نویسندگان

  • De-Qi Xiao
  • Pei-Hong Xu
  • Hui Deng
  • Li-Sha Chen
  • Xu-An Ding
  • Mei Bai
  • Pei Li
  • Ding-Fen Yuan
چکیده

Objective: To investigate the activation of the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway in the peripheral T cells of patients with atopic dermatitis (AD) and to explore its clinical significance. Methods: Peripheral T lymphocytes were isolated with a T cell isolation kit; PI3K expression was detected by immunoprecipitation and with an enzyme-linked immunosorbent assay (ELISA); Akt and its phosphorylation were analyzed with western blotting; T cell proliferation was analyzed with the MTT method; and interleukin (IL)-6 and IL-10 levels were detected with ELISA. Results: PI3K and p-Akt/Akt expression in freshly prepared peripheral T cells from AD patients were significantly higher than those in healthy controls (P < 0.05). When T cells from healthy controls were incubated with sera from AD patients for 24 hours, their PI3K and p-Akt/Akt expression significantly increased (P < 0.05). Treatment with the PI3K inhibitor LY294002 combined with a CD3/CD28 monoclonal antibody (mAb) significantly reduced the CD3/CD28 mAb-induced proliferation of T cells (195% ± 28% vs. 125% ± 22%, P < 0.05), IL-6 secretion (823 ± 128 ng/L vs. 431 ± 64 ng/L, P < 0.05), and IL-10 secretion (213 ± 35 ng/L vs. 120 ± 21 ng/L, P < 0.05) in AD patients. In addition, the PI3K and p-Akt/Akt protein levels in freshly prepared peripheral T cells from AD patients were unrelated to the patients’ Eczema Area and Severity Index (EASI). Conclusion: The PI3K/Akt signaling pathway is abnormally activated in peripheral T cells from AD patients, and its activation corresponds to T cell proliferation and cytokine secretion, suggesting that serum cytokines that activate this pathway may be present in the peripheral blood of AD patients.

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تاریخ انتشار 2017