The present study aimed to investigate the existence of immunoregulation‑associated long non‑coding (lnc)RNAs mediated by T lymphocytes in the wound surfaces of diabetic foot ulcers (DFUs). The wound skin tissues of patients receiving debridement for trauma or DFUs associated with infection were obtained. Dermatological histological changes were observed by pathological staining, and T lymphocyte subsets and inflammation‑associated cytokines were identified. Gene chip technology was used to screen for lncRNAs regulated by immune cells. The wound skin structure in the control group was revealed to be complete, and the inflammatory response was not marked. However, the wound skin structure in the ulcer group was disordered and exhibited a notable inflammatory response. Compared with the control group, expression levels of cluster of differentiation (CD)3 and CD8 in the wound surface tissues of the ulcer group were significantly increased, while the expression levels of interleukin (IL)‑1β, IL‑2, IL‑10, interferon‑γ and tumor necrosis factor‑α were significantly upregulated. A target regulatory association was identified between downregulated lncRNA‑ENST00000411554 and upregulated mitogen‑activated protein kinase (MAPK)1 in DFU tissues, and a negative correlation was detected between this RNA and protein. The present results suggested that an immune functional disorder of T lymphocytes may be closely associated with the development of DFUs. Furthermore, activation of the MAPK signal transduction pathway mediated by the lncRNA‑ENST00000411554/MAPK1 axis may affect the DFU immune regulatory imbalance.
Keywords: diabetic foot ulcers; T lymphocytes; long non-coding RNA; mitogen-activated protein kinase signaling pathway.