B7-H1-Induced Apoptosis as a Mechanism of Immune Privilege of Corneal Allografts
Open accessAbstract
The programmed death-1 (PD-1) costimulatory pathway has been demonstrated to play a role in the regulation of immune responses and peripheral tolerance. We investigated the role of this pathway in establishing an immune privilege status of corneal allografts in mice. B7-H1, but not B7-DC or PD-1, was expressed constitutively in the eye, i.e., cornea, iris-ciliary body, and retina. After corneal allografting, PD-1+CD4+ T cells infiltrated and adhered with B7-H1+ corneal endothelium. Blockade of PD-1 or B7-H1, but not B7-DC, led to accelerated corneal allograft rejection. In B7-H1-expressing corneal allografts, apoptosis of the infiltrating PD-1+CD4+ or CD8+ T cells was observed, after which there was allograft acceptance. In contrast, B7-H1 blockade suppressed apoptosis of infiltrating PD-1+ T cells, which led to allograft rejection. In vitro, destruction of corneal endothelial cells by alloreactive T cells was enhanced when the cornea was pretreated with anti-B7-H1 Ab. This is the first demonstration that the constitutive expression of B7-H1 plays a critical role in corneal allograft survival. B7-H1 expressed on corneal endothelial cells maintains long-term acceptance of the corneal allografts by inducing apoptosis of effector T cells within the cornea.
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Active local or peripheral tolerance can be induced through conversion of T cells to regulatory T cells or apoptosis of infiltrated effector T cells by inhibitory molecules expressed on the retinal pigmented epithelium or resident stromal cells.
“An active local or peripheral tolerance to prevent runaway immune responses can be induced in some cases through the conversion of T cell to regulatory T cells (Treg) or the apoptosis of infiltrated effector T cells by inhibitory molecules expressed on the retinal pigmented epithelium (RPE) or resident stromal cells [9][10][11].”
From Risk mitigation of immunogenicity: a key to personalized retinal gene therapy (2021) · cites this paper as [11]
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- Authors
- Hori, J., Wang, M., Miyashita, M., Tanemoto, K., Takahashi, H., Takemori, T., Okumura, K., Yagita, H., & Azuma, M.
- Affiliations
- Nippon Medical School (JP)
- National Institute of Infectious Diseases (JP)
- Juntendo University (JP)
- Department of Immunology, Juntendo University School of Medicine , Tokyo ,
- Tokyo Medical and Dental University (JP)
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2006-11-01
- Volume
- 177
- Issue
- 9
- Pages
- 5928-5935
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2150372796
- Cited by
- 208
- References
- 58
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 4 · 2023: 3 · 2022: 7 · 2021: 11 · 2020: 16 · 2019: 8 · 2018: 10 · 2017: 8 · 2016: 12 · 2015: 10 · 2014: 7 · 2013: 18 · 2012: 7
- FWCI
- 5.76
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Corneal surgery and disorders
- Health Sciences › Medicine › Surgery › Transplantation: Methods and Outcomes
- Keywords
- PD-L1, PD-1, immune privilege, corneal allograft, corneal endothelium, T cell apoptosis, allograft rejection, costimulatory molecules, PD-L2, CD4+ T cells, CD8+ T cells
- MeSH terms
- Animals, Antibodies, Monoclonal, Antigens, Surface, Cornea, Graft Rejection, Graft Survival, Male, Membrane Glycoproteins, Mice, Inbred Strains, Peptides, Transplantation, Homologous, CD4-Positive T-Lymphocytes, Corneal Transplantation, Apoptosis, B7-1 Antigen, CD8-Positive T-Lymphocytes, Endothelial Cells, Apoptosis Regulatory Proteins, Mice, B7-H1 Antigen, Programmed Cell Death 1 Receptor, Programmed Cell Death 1 Ligand 2 Protein
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