The role of PD-1/PD-L1 pathway in ulcerative colitis and changes following tonsil-derived mesenchymal stem cells treatment.

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  • Additional Information
    • Source:
      Publisher: Korean Association of Internal Medicine Country of Publication: Korea (South) NLM ID: 8712418 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2005-6648 (Electronic) Linking ISSN: 12263303 NLM ISO Abbreviation: Korean J Intern Med Subsets: MEDLINE
    • Publication Information:
      Original Publication: [Seoul] : Korean Association of Internal Medicine
    • Subject Terms:
      Colitis, Ulcerative*/therapy ; Colitis, Ulcerative*/metabolism ; Colitis, Ulcerative*/immunology ; Colitis, Ulcerative*/pathology ; B7-H1 Antigen*/metabolism ; Programmed Cell Death 1 Receptor*/metabolism ; Mesenchymal Stem Cell Transplantation* ; Disease Models, Animal* ; Colon*/metabolism ; Colon*/pathology ; Palatine Tonsil*/pathology ; Palatine Tonsil*/metabolism ; Palatine Tonsil*/immunology; Humans ; Animals ; Male ; Female ; Intestinal Mucosa/metabolism ; Intestinal Mucosa/pathology ; Signal Transduction ; Adult ; Case-Control Studies ; Mesenchymal Stem Cells/metabolism ; Middle Aged ; Treatment Outcome ; Mice, Inbred C57BL
    • Abstract:
      Background/aims: The programmed death 1 (PD-1)/programmed death-ligand 1 (PD-L1) pathway has not been fully evaluated in inflammatory bowel disease. We evaluated PD-1/PD-L1 levels in patients with ulcerative colitis (UC) and their significance in tonsil-derived mesenchymal stem cells (TMSCs) treatment.
      Methods: Using acute and chronic murine colitis model, we measured the PD-1 and PD-L1 levels in inflamed colonic tissues pre- and post-treatment with TMSCs. We also measured PD-1 and PD-L1 levels in colonic tissues from UC patients, compared to normal controls.
      Results: In the analysis using human colonic tissues, a significant increase in the levels of PD-1 and PD-L1 was observed in the colonic mucosa of patients with UC compared with normal controls (p < 0.001 and p = 0.005, respectively). When comparing the maximal disease extent, PD-L1 levels were highest in patients with proctitis (38.5 ± 46.7), followed by left-side colitis (17.5 ± 23.1) and extensive colitis (5.2 ± 8.2) (p < 0.001). In the chronic colitis model, the level of PD-L1 was decreased (p = 0.040) and the level of PD-1 increased more than in normal controls (p = 0.047). After treatment with TMSC, significant improvements were observed in body weight, disease activity index, and colon length recovery. Additionally, the levels of PD-1 and PD-L1 were recovered; PD-L1 significantly increased (p = 0.031), while the level of PD-1 decreased (p = 0.310).
      Conclusion: The altered expression of PD-1 and PD-L1 in colonic mucosa may be a possible mechanism of UC, and T-MSC-derived PD-L1 could help suppress colitis.
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    • Grant Information:
      Ewha Womans University; 2020R1I1A1A01073545 National Research Foundation of Korea; 2019R1A2C1002526 National Research Foundation of Korea; 2022R1H1A2091616 National Research Foundation of Korea; Ministry of Education
    • Contributed Indexing:
      Keywords: Colitis model; Colonic mucosa; Human colonic tissues; Inflammatory bowel disease
    • Accession Number:
      0 (B7-H1 Antigen)
      0 (Programmed Cell Death 1 Receptor)
      0 (CD274 protein, human)
      0 (PDCD1 protein, human)
      0 (Cd274 protein, mouse)
      0 (Pdcd1 protein, mouse)
    • Publication Date:
      Date Created: 20241117 Date Completed: 20241117 Latest Revision: 20241120
    • Publication Date:
      20241120
    • Accession Number:
      PMC11569929
    • Accession Number:
      10.3904/kjim.2024.019
    • Accession Number:
      39551070