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The Immunoregulatory Role of Programmed Death-Ligand 1 in Wound Healing Dynamics | ||
| Iranian Journal of Immunology | ||
| دوره 22، شماره 4، اسفند 2025، صفحه 357-360 | ||
| نوع مقاله: Letter To The Editor | ||
| شناسه دیجیتال (DOI): 10.22034/iji.2025.107588.3070 | ||
| نویسندگان | ||
| Mohammad Hasan Soheilifar* 1؛ Hoda Keshmiri Neghab1؛ Sima Nobari2 | ||
| 1Department of Medical Laser, Medical Laser Research Center, Yara Institute, ACECR, Tehran, Iran. | ||
| 2Gastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran. | ||
| چکیده | ||
| Wound healing is a complex and dynamic process that encompasses four interrelated phases: hemostasis, inflammation, proliferation, and remodeling. Inflammation plays a pivotal role in both acute and chronic wound healing. In chronic diabetic wounds, the normal healing rate is impaired due to persistent inflammation, which is associated with unbalanced immune responses. Microbial biofilms, increased immune cell activity, the accumulation of pro-inflammatory cytokines, and free radicals can contribute to the establishment of chronic inflammation in these wounds. Modulating the immune microenvironment in chronic wounds can significantly enhance the process of wound healing and tissue regeneration. Programmed death-ligand 1 (PD-L1) is an important immune checkpoint molecule that can bind to the PD-1 receptor on the immune cells and suppress the immunogenic responses. Although inflammation plays a significant role in wound healing, the role of PD-L1 in chronic wounds is not clearly understood. Interestingly, recent evidence indicates that fibroblast cells in granulation tissues express PD-L1. This paper will review the current findings and potential advantages of PD-L1 in the wound healing process, presenting a novel approach for treating chronic wounds. | ||
| کلیدواژهها | ||
| Immune checkpoint؛ Inflammation؛ PD-L1؛ Wound Healing | ||
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آمار تعداد مشاهده مقاله: 125 تعداد دریافت فایل اصل مقاله: 83 |
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