It has been over 70 years since Peter Medawar called the eye immune privileged based on the prolonged survival of allographs within the ocular microenvironment. Over this time, we have come to understand that this unique relationship between the ocular microenvironment and the immune system involves both local and systemic mechanisms of immune suppression and tolerance. This includes a physical blood barrier and lack of direct lymphatics. There are molecules both soluble and membrane-bound expressed by the cells of the ocular microenvironment that suppress immune cells from responding to triggers of inflammation, while they can promote activation of suppressor cells and T regulatory cells. Additionally, ocular immune privilege has the ability to induce systemic tolerance to antigens placed within the eye through the phenomena of anterior chamber associated immune deviation (ACAID). These mechanisms work together to suppress the activation of inflammation within the eye to protect its delicate structure from permanent damage by uncontrolled inflammatory responses.
The majority of the studies of retinal immunobiology have been on immune privilege, transplantation, and infection. From these studies, it is clear that the retina has adapted several molecules such as CD200, CTLA2, CX3CL1, TGF-2, TRAIL, FasL and neuropeptides to inhibit microglial cell, infiltrating T cells and macrophages cells from responding to signals of inflammation, and to generate pro-inflammatory cytokines. In addition, these same molecules promote anti-inflammatory activity, and immune tolerance in immune cells. As more is understood about these molecular mechanisms of ocular immune privilege in manipulating immune cell activity and the process of inflammation, new questions are being asked about how ocular immune privilege is maintained under chronic stress conditions such as aging and diabetes. There is a potential role for inflammation and immune cells in retinopathies involving ischemia, cardiovascular disease, and in age-related macular degeneration (AMD). It is not clear if the molecular mechanisms that preserve the eye free from inflammation contribute or could help to prevent the pathology of other retinopathies.
This issue, entitled Retinal Immunobiology and Retinopathy, will cover areas of traditional immunology studies into retinal immune privilege, autoimmunity, and infection, and will expand this discussion into retinopathies caused by aging (i.e., AMD), diabetes, and glaucoma where evidence is emerging that inflammation and immune cells may have a role in the development or progression of these retinal diseases. Also welcomed are manuscripts that use the mechanism of ocular immune privilege to control retinopathy and autoimmune disease, demonstrating the effectiveness of the molecules of ocular immune privilege to block unwanted inflammation.
Topic Editor Andrew Taylor has a sponsored research agreement and is a consultant with Palatin Technologies Inc. in Cranbury, New Jersey. All other Topic Editors declare no competing interests with regards to the Research Topic subject.
It has been over 70 years since Peter Medawar called the eye immune privileged based on the prolonged survival of allographs within the ocular microenvironment. Over this time, we have come to understand that this unique relationship between the ocular microenvironment and the immune system involves both local and systemic mechanisms of immune suppression and tolerance. This includes a physical blood barrier and lack of direct lymphatics. There are molecules both soluble and membrane-bound expressed by the cells of the ocular microenvironment that suppress immune cells from responding to triggers of inflammation, while they can promote activation of suppressor cells and T regulatory cells. Additionally, ocular immune privilege has the ability to induce systemic tolerance to antigens placed within the eye through the phenomena of anterior chamber associated immune deviation (ACAID). These mechanisms work together to suppress the activation of inflammation within the eye to protect its delicate structure from permanent damage by uncontrolled inflammatory responses.
The majority of the studies of retinal immunobiology have been on immune privilege, transplantation, and infection. From these studies, it is clear that the retina has adapted several molecules such as CD200, CTLA2, CX3CL1, TGF-2, TRAIL, FasL and neuropeptides to inhibit microglial cell, infiltrating T cells and macrophages cells from responding to signals of inflammation, and to generate pro-inflammatory cytokines. In addition, these same molecules promote anti-inflammatory activity, and immune tolerance in immune cells. As more is understood about these molecular mechanisms of ocular immune privilege in manipulating immune cell activity and the process of inflammation, new questions are being asked about how ocular immune privilege is maintained under chronic stress conditions such as aging and diabetes. There is a potential role for inflammation and immune cells in retinopathies involving ischemia, cardiovascular disease, and in age-related macular degeneration (AMD). It is not clear if the molecular mechanisms that preserve the eye free from inflammation contribute or could help to prevent the pathology of other retinopathies.
This issue, entitled Retinal Immunobiology and Retinopathy, will cover areas of traditional immunology studies into retinal immune privilege, autoimmunity, and infection, and will expand this discussion into retinopathies caused by aging (i.e., AMD), diabetes, and glaucoma where evidence is emerging that inflammation and immune cells may have a role in the development or progression of these retinal diseases. Also welcomed are manuscripts that use the mechanism of ocular immune privilege to control retinopathy and autoimmune disease, demonstrating the effectiveness of the molecules of ocular immune privilege to block unwanted inflammation.
Topic Editor Andrew Taylor has a sponsored research agreement and is a consultant with Palatin Technologies Inc. in Cranbury, New Jersey. All other Topic Editors declare no competing interests with regards to the Research Topic subject.
