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Molecular mechanisms of immune privilege of the cornea – as a potential of Immune checkpoint therapy
Author(s) -
Hori J.
Publication year - 2016
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2016.0231
Subject(s) - immune privilege , cornea , immune system , microbiology and biotechnology , corneal transplantation , biology , fas ligand , immunology , effector , il 2 receptor , t cell , apoptosis , programmed cell death , neuroscience , genetics
Summary The eye, which is endowed with immune privilege, is a rare organ that permits analysis of the regulatory mechanisms for inflammation in organs. In particular, studies using animal models of corneal transplantation have revealed the molecular mechanisms of corneal cell‐mediated immune privilege. Several molecules expressed in the cornea induce apoptosis of T cells and delete effector T cells in the cornea. Constitutive expression of Fas ligand and programed death ligand 1 (PD‐L1, B7‐H1) on corneal endothelial cells induce apoptosis of effector T cells via Fas and PD‐1, respectively. B7‐H3 is also constitutively expressed in the corneal endothelium and iris cilialy body and plays a role in the induction of anterior chamber associated immune deviation (ACAID). We have also found that constitutive expression of glucocorticoid‐induced TNF receptor family‐related protein ligand (GITRL) in the cornea mediates local expansion of CD25+CD4+T regulatory cells and suppresses conventional effector T cell function via GITR. These differently functioning molecules contribute to the local immune suppressive microenvironment in the cornea. The study for the roles of B7RP‐1 and Galectine‐9 expressed in the cornea are also introduced.