CD95-Induced Apoptosis of Lymphocytes in an Immune Privileged Site Induces Immunological Tolerance
Open accessAbstract
We examined the relationship between cell death and tolerance induction following antigen injection into the anterior chamber of the eye. Our data show that when inflammatory cells undergo apoptosis following infection with HSV-1, tolerance to the virus was observed. In contrast, when cell death was absent due to defects in Fas or FasL, immune tolerance was not observed. Further studies revealed that cell death and tolerance required that the lymphoid cells be Fas+ and the eye be FasL+. Additionally, we show that while Fas/FasL-mediated apoptosis occurred in the eye, it was apoptotic cell death that was critical for tolerance induction. Our results further demonstrate immune privilege is not a passive process involving physical barriers, but is an active process that employs an important natural mechanism to induce cell death and immune tolerance.
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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 [10]
Tolerance induction by apoptotic cells depends on MHC class I molecules and involves immune suppression by CD8+ T cells.
“Perhaps paradoxically, tolerance induction by apoptotic cells depends on MHC class I molecules and involves immune suppression by CD8+ T cells10,24,25.”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [10]
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References 41 · Cited by 382
- Authors
- Griffith, T. S., Yu, X., Herndon, J. M., Green, D. R., & Ferguson, T. A.
- Affiliations
- Washington University in St. Louis (US)
- La Jolla Institute for Immunology (US)
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 1996-07
- Volume
- 5
- Issue
- 1
- Pages
- 7-16
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2060820237
- Cited by
- 382
- References
- 41
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 1 · 2023: 5 · 2022: 2 · 2021: 3 · 2020: 4 · 2019: 1 · 2018: 3 · 2017: 3 · 2016: 3 · 2015: 5 · 2014: 1 · 2013: 4 · 2012: 8
- FWCI
- 13.97
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Eye Institute (EY 06374, EY06765)
- National Institute of General Medical Sciences (GM-52735)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- Fas, Fas ligand, apoptosis, immune privilege, immune tolerance, anterior chamber of the eye, herpes simplex virus type 1, lymphocytes, ocular immunology, Fas/FasL signaling
- MeSH terms
- Animals, Eye, Immune Tolerance, Ligands, Lymphocytes, Membrane Glycoproteins, Mice, Inbred C57BL, Mice, Mutant Strains, Mice, Transgenic, Radiation Chimera, Bone Marrow Transplantation, Apoptosis, Herpesvirus 1, Human, fas Receptor, Mice, Fas Ligand Protein
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