ArticleThe Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation2013
Anti-major histocompatibility complex-induced obliterative airway disease: selective role for CD4 and CD8 T cells in inducing immune responses to self-antigens.
Article in The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- 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
- Advanced Role of Neutrophils in Common Respiratory Diseases.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
- NFAT5/STAT3 interaction mediates synergism of high salt with IL-17 towards induction of VEGF-A expression in breast cancer cells.Oncology letters · 2016Article
- B Cell-Activating Transcription Factor Plays a Critical Role in the Pathogenesis of Anti-Major Histocompatibility Complex-Induced Obliterative Airway Disease.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2016Article
- Role of defensins in the pathogenesis of chronic lung allograft rejection.Human immunology · 2014Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe goal of this study was to define the role of T-cell sub-sets in the pathogenesis of autoimmunity-induced obliterative airway disease by passive transfer of CD8+ or CD4+ T cells.
methodsAntibodies to major histocompatibility complex (MHC) class I were administered intrabronchially into C57BL/6 animals. Lungs were analyzed by histopathology and immunohistochemistry. The CD8+ and CD4+ T-cell sub-sets were purified from the lung-infiltrating cells and intrabronchially transferred. Frequency of cells secreting interleukin-17, interferon-γ, or interleukin-10 to self-antigens was enumerated by enzyme-linked immunospot assay. Myeloperoxidase and antibodies to self-antigens were determined by enzyme-linked immunosorbent assay. Cytokine and growth factor expression was determined by quantitative reverse-transcription polymerase chain reaction.
resultsPassive transfer of lung-infiltrating CD8 T cells isolated after anti-MHC class I administration, along with sub-optimal dose, induced significantly higher cellular infiltration (89.3% ± 7.9% vs 62.8% ± 10.1%, p < 0.05) vs the CD4 transfer group. Further, passive transfer of CD8 cells resulted in infiltration of neutrophils and macrophages, suggesting early injury response. In contrast, passive transfer of CD4+ T cells induced a significantly higher degree of luminal occlusion (29.3% ± 5.6% vs 8.6 ± 2.5%, p < 0.05) and fibrosis (54.4% ± 9.3% vs 10.2% ± 2.4%, p < 0.05) vs the CD8 group and B-cell infiltration, leading to immune responses to lung-associated self-antigens and fibrosis.
conclusionLigation of MHC molecules by its specific antibodies induced early injury with neutrophils, macrophages, and CD8 T cells, which leads to exposure of cryptic self-antigens and their presentation by the infiltrating CD4+ T cells and B cells, leading to the development of immune responses to self-antigens and culminating in obliterative airway disease.
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