ArticleClinical and experimental immunology2012
A shift in the collagen V antigenic epitope leads to T helper phenotype switch and immune response to self-antigen leading to chronic lung allograft rejection.
Article in Clinical and experimental immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Pooled it
- Temporal Dynamics of Pulmonary Fibrosis and Immune Dysregulation in a Collagen V-Driven Systemic Sclerosis Model.International journal of molecular sciences · 2025Article
- [Immunological Aspects after Lung Transplantation].Zentralblatt fur Chirurgie · 2025Review
- Markers of Bronchiolitis Obliterans Syndrome after Lung Transplant: Between Old Knowledge and Future Perspective.Biomedicines · 2022Review
- Immune processes in the pathogenesis of chronic lung allograft dysfunction: identifying the missing pieces of the puzzle.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Extracellular Vesicles Mediate Immune Responses to Tissue-Associated Self-Antigens: Role in Solid Organ Transplantations.Frontiers in immunology · 2022Review
- Microvascular Inflammation of the Renal Allograft: A Reappraisal of the Underlying Mechanisms.Frontiers in immunology · 2022Review
- Antithymocyte globulin is associated with a lower incidence of de novo donor-specific antibody detection in lung transplant recipients: A single-center experience.Immunity, inflammation and disease · 2021Article
- Immune Checkpoints Expression in Chronic Lung Allograft Rejection.Frontiers in immunology · 2021Article
- Chronic lung allograft dysfunction post-lung transplantation: The era of bronchiolitis obliterans syndrome and restrictive allograft syndrome.World journal of transplantation · 2020Review
- Adipose-derived stem cells and adipose-derived stem cell-conditioned medium modulate in situ imbalance between collagen I- and collagen V-mediated IL-17 immune response recovering bleomycin pulmonary fibrosis.Histology and histopathology · 2020Article
- Identification of Autoimmunity to Peptides of Collagen V α1 Chain as Newly Biomarkers of Early Stage of Systemic Sclerosis.Frontiers in immunology · 2020Article
- Community-acquired Respiratory Viruses Are a Risk Factor for Chronic Lung Allograft Dysfunction.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2019Article
- The role of donor-derived exosomes in lung allograft rejection.Human immunology · 2019Review
- High salt induces P-glycoprotein mediated treatment resistance in breast cancer cells through store operated calcium influx.Oncotarget · 2018Article
- Potential anticancer effect of prostratin through SIK3 inhibition.Oncology letters · 2018Article
- Not All Antibodies Are Created Equal: Factors That Influence Antibody Mediated Rejection.Journal of immunology research · 2017Review
- Critical role of SIK3 in mediating high salt and IL-17 synergy leading to breast cancer cell proliferation.PloS one · 2017Article
- Lung Injury and Loss of Regulatory T Cells Primes for Lung-Restricted Autoimmunity.Critical reviews in immunology · 2017Review
- The importance of non-HLA antibodies in transplantation.Nature reviews. Nephrology · 2016Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Immune responses to human leucocyte antigen (HLA) and self-antigen collagen V (Col-V) have been proposed in the pathogenesis of chronic rejection (bronchiolitis obliterans syndrome, BOS) following human lung transplantation (LTx). In this study, we defined the role for the shift in immunodominant epitopes of Col-V in inducing T helper phenotype switch leading to immunity to Col-V and BOS. Sera and lavage from BOS(+) LTx recipients with antibodies to Col-V were analysed. Two years prior to BOS, patients developed antibodies to both Col-V,α1(V) and α2(V) chains. However, at clinical diagnosis of BOS, antibodies became restricted to α1(V). Further, lung biopsy from BOS(+) patients bound to antibodies to α1(V), indicating that these epitopes are exposed. Fourteen Col-V peptides [pep1-14, pep1-4 specific to α1(V), pep5-8 to α1,2(V) and pep9-14 to α2(V)] which bind to HLA-DR4 and -DR7, demonstrated that prior to BOS, pep 6, 7, 9, 11 and 14 were immunodominant and induced interleukin (IL)-10. However, at BOS, the response switched to pep1, 4 and 5 and induced interferon (IFN)-γ and IL-17 responses, but not IL-10. The T helper (Th) phenotype switch is accompanied by decreased frequency of regulatory T cells (T(regs) ) in the lavage. LTx recipients with antibodies to α1(V) also demonstrated increased matrix metalloproteinase (MMP) activation with decreased MMP inhibitor, tissue inhibitor of metalloproteinase (TIMP), suggesting that MMP activation may play a role in the exposure of new Col-V antigenic epitopes. We conclude that a shift in immunodominance of self-antigenic determinants of Col-V results in induction of IFN-γ and IL-17 with loss of tolerance leading to autoimmunity to Col-V, which leads to chronic lung allograft rejection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.