Newswise, February 5, 2016 — Potential new approaches to
treating eye diseases such as age-related macular degeneration (AMD) are
described in a new study, “IL-33 amplifies an innate immune response in the
degenerating retina,” in the February Journal of Experimental Medicine.
AMD is a leading cause of vision impairment in old age, and is
caused by the degeneration of cells in the retinal layer of the eye.
Retinal
cell death can be induced by phagocytic immune cells that infiltrate the tissue
in response to injury or infection, but the molecular signals that trigger
phagocyte invasion are largely unknown. A team of researchers led by Hongkang
Xi and Menno van Lookeren Campagne, of the Department of Immunology at
Genentech, Inc., in South San Francisco, Calif., discovered that a
pro-inflammatory signaling protein, or cytokine, called IL-33, plays a key role
in recruiting phagocytes to damaged retina and inducing retinal degeneration.
Working with rats and mice,
Xi and colleagues found that
specialized retinal cells called Müller glial cells release IL-33 in response
to retinal injury. The cytokine then binds to its receptor on the surface of
the Müller cells and induces the release of additional inflammatory proteins
that attract phagocytes to the damaged retina. Blocking the IL-33 receptor
inhibited this process and prevented injury-induced retinal degeneration.
The researchers also found that IL-33 levels are increased in
the retinas of AMD patients, suggesting that the same pathway may occur in
humans. Inhibiting IL-33 may therefore help treat AMD and other retinal
degenerative diseases.
“This study for the first time shows increased expression of
IL-33 in AMD and further demonstrates a role for glia-derived IL-33 in the
accumulation of myeloid cells in the outer retina, loss of photoreceptors, and
functional impairment of the retina in preclinical models of retina stress,”
the authors note.
© 2016 Xi et al. J Exp. Med.http://www.dx.doi.org/10.1084/jem.20150894
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About The Journal of Experimental Medicine
The Journal of Experimental Medicine (JEM) is published by The Rockefeller University Press. All editorial decisions on manuscripts submitted are made by research-active scientists in conjunction with our in-house scientific editors.JEM provides free online access to many article types immediately, with complete archival content freely available online since the journal's inception. Authors retain copyright of their published works, and third parties may reuse the content for non-commercial purposes under a creative commons license. For more information, please visit jem.org.
The Journal of Experimental Medicine (JEM) is published by The Rockefeller University Press. All editorial decisions on manuscripts submitted are made by research-active scientists in conjunction with our in-house scientific editors.JEM provides free online access to many article types immediately, with complete archival content freely available online since the journal's inception. Authors retain copyright of their published works, and third parties may reuse the content for non-commercial purposes under a creative commons license. For more information, please visit jem.org.
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