Cargando…
Induction of Immune Surveillance of the Dysmorphogenic Lens
The lens has been considered to be an immune privileged site not susceptible to the immune processes normally associated with tissue injury and wound repair. However, as greater insight into the immune surveillance process is gained, we have reevaluated the concept of immune privilege. Our studies u...
Autores principales: | , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5701161/ https://www.ncbi.nlm.nih.gov/pubmed/29176738 http://dx.doi.org/10.1038/s41598-017-16456-5 |
_version_ | 1783281280981401600 |
---|---|
author | Logan, Caitlin M. Bowen, Caitlin J. Menko, A. Sue |
author_facet | Logan, Caitlin M. Bowen, Caitlin J. Menko, A. Sue |
author_sort | Logan, Caitlin M. |
collection | PubMed |
description | The lens has been considered to be an immune privileged site not susceptible to the immune processes normally associated with tissue injury and wound repair. However, as greater insight into the immune surveillance process is gained, we have reevaluated the concept of immune privilege. Our studies using an N-cadherin lens-specific conditional knockout mouse, N-cad(Δlens), show that loss of this cell-cell junctional protein leads to lens degeneration, necrosis and fibrotic change, postnatally. The degeneration of this tissue induces an immune response resulting in immune cells populating the lens that contribute to the development of fibrosis. Additionally, we demonstrate that the lens is connected to the lymphatic system, with LYVE(+) labeling reaching the lens along the suspensory ligaments that connect the lens to the ciliary body, providing a potential mechanism for the immune circulation. Importantly, we observe that degeneration of the lens activates an immune response throughout the eye, including cornea, vitreous humor, and retina, suggesting a coordinated protective response in the visual system to defects of a component tissue. These studies demonstrate that lens degeneration induces an immune response that can contribute to the fibrosis that often accompanies lens dysgenesis, a consideration for understanding organ system response to injury. |
format | Online Article Text |
id | pubmed-5701161 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-57011612017-11-30 Induction of Immune Surveillance of the Dysmorphogenic Lens Logan, Caitlin M. Bowen, Caitlin J. Menko, A. Sue Sci Rep Article The lens has been considered to be an immune privileged site not susceptible to the immune processes normally associated with tissue injury and wound repair. However, as greater insight into the immune surveillance process is gained, we have reevaluated the concept of immune privilege. Our studies using an N-cadherin lens-specific conditional knockout mouse, N-cad(Δlens), show that loss of this cell-cell junctional protein leads to lens degeneration, necrosis and fibrotic change, postnatally. The degeneration of this tissue induces an immune response resulting in immune cells populating the lens that contribute to the development of fibrosis. Additionally, we demonstrate that the lens is connected to the lymphatic system, with LYVE(+) labeling reaching the lens along the suspensory ligaments that connect the lens to the ciliary body, providing a potential mechanism for the immune circulation. Importantly, we observe that degeneration of the lens activates an immune response throughout the eye, including cornea, vitreous humor, and retina, suggesting a coordinated protective response in the visual system to defects of a component tissue. These studies demonstrate that lens degeneration induces an immune response that can contribute to the fibrosis that often accompanies lens dysgenesis, a consideration for understanding organ system response to injury. Nature Publishing Group UK 2017-11-24 /pmc/articles/PMC5701161/ /pubmed/29176738 http://dx.doi.org/10.1038/s41598-017-16456-5 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Logan, Caitlin M. Bowen, Caitlin J. Menko, A. Sue Induction of Immune Surveillance of the Dysmorphogenic Lens |
title | Induction of Immune Surveillance of the Dysmorphogenic Lens |
title_full | Induction of Immune Surveillance of the Dysmorphogenic Lens |
title_fullStr | Induction of Immune Surveillance of the Dysmorphogenic Lens |
title_full_unstemmed | Induction of Immune Surveillance of the Dysmorphogenic Lens |
title_short | Induction of Immune Surveillance of the Dysmorphogenic Lens |
title_sort | induction of immune surveillance of the dysmorphogenic lens |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5701161/ https://www.ncbi.nlm.nih.gov/pubmed/29176738 http://dx.doi.org/10.1038/s41598-017-16456-5 |
work_keys_str_mv | AT logancaitlinm inductionofimmunesurveillanceofthedysmorphogeniclens AT bowencaitlinj inductionofimmunesurveillanceofthedysmorphogeniclens AT menkoasue inductionofimmunesurveillanceofthedysmorphogeniclens |