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Related Experiment Video

Updated: Oct 21, 2025

Trans-vivo Delayed Type Hypersensitivity Assay for Antigen Specific Regulation
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Immune Checkpoints Expression in Chronic Lung Allograft Rejection.

Ilaria Righi1, Valentina Vaira2,3, Letizia Corinna Morlacchi4

  • 1Thoracic Surgery and Lung Transplantation Unit, Fondazione IRCCS Ca' Granda-Ospedale Maggiore Policlinico, Milan, Italy.

Frontiers in Immunology
|September 7, 2021
PubMed
Summary

Immune checkpoint molecules like PD-1 and CTLA-4 are altered in chronic lung allograft dysfunction (CLAD), particularly in restrictive allograft syndrome (RAS). This suggests a role in rejection and potential therapeutic targets for lung transplant patients.

Keywords:
FoxP3PD-1 and PD-L1Treg lymphocyteschronic rejectionimmunologylung transplant

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Area of Science:

  • Immunology
  • Transplantation Science
  • Oncology (Immuno-oncology principles)

Background:

  • Chronic lung allograft dysfunction (CLAD) significantly impacts lung transplant recipient survival and quality of life.
  • While various immune factors in CLAD are studied, immune checkpoint molecule expression remains largely uninvestigated, especially differentiating between BOS and RAS subtypes.

Purpose of the Study:

  • To analyze the expression and function of immune checkpoint molecules in lung allografts affected by CLAD, comparing bronchiolitis obliterans syndrome (BOS) and restrictive allograft syndrome (RAS).
  • To explore the potential role of these molecules in graft rejection and prognosis.

Main Methods:

  • Observational study analyzing eight explanted lung allografts from patients with CLAD (re-transplanted) and six control lungs.
  • Immunohistochemistry was used to assess the expression of PD-1, PD-L1, CTLA-4, CD4, CD8, FOXP3, TIGIT, TOX, and B-cell-specific activator protein.

Main Results:

  • Restrictive allograft syndrome (RAS) allografts showed an inverted CD4/CD8 ratio compared to bronchiolitis obliterans syndrome (BOS) allografts.
  • RAS grafts exhibited higher percentages of T lymphocytes expressing PD-1, PD-L1, and CTLA-4.
  • A significant reduction in exhausted T lymphocytes (PD-1+/TOX+) and exhausted regulatory T cells (PD-1+/FOXP3+) was observed in RAS compared to BOS.

Conclusions:

  • Immune checkpoint molecules likely play a role in chronic lung allograft rejection, offering an immunological basis for the poorer prognosis in RAS.
  • Monitoring immune checkpoints may provide prognostic value for detecting rejection onset in lung transplant recipients.
  • Modulating immune checkpoint function could be a potential therapeutic strategy for managing chronic rejection post-lung transplantation.