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Characterization of Tear Immunoglobulins in a Small-Cohort of Keratoconus Patients
Keratoconus (KC) is classically considered a non-inflammatory condition caused by central corneal thinning that leads to astigmatism and reduced visual acuity. Previous studies have identified increased systemic levels of pro-inflammatory factors, including interleukin-6, tumor necrosis factor-α, an...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7287105/ https://www.ncbi.nlm.nih.gov/pubmed/32523038 http://dx.doi.org/10.1038/s41598-020-66442-7 |
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author | McKay, Tina B. Serjersen, Henrik Hjortdal, Jesper Zieske, James D. Karamichos, Dimitrios |
author_facet | McKay, Tina B. Serjersen, Henrik Hjortdal, Jesper Zieske, James D. Karamichos, Dimitrios |
author_sort | McKay, Tina B. |
collection | PubMed |
description | Keratoconus (KC) is classically considered a non-inflammatory condition caused by central corneal thinning that leads to astigmatism and reduced visual acuity. Previous studies have identified increased systemic levels of pro-inflammatory factors, including interleukin-6, tumor necrosis factor-α, and matrix metalloproteinase-9, suggesting that KC may have an inflammatory component in at least a subset of patients. In this study, we evaluated the levels of different immunoglobulins (light and heavy chains) based on Ig α, Ig λ, Ig κ, Ig µ, and Ig heavy chain subunits in non-KC tears (n = 7 control individuals) and KC tears (n = 7 KC patients) using tandem-liquid chromatography mass spectrometry. The most abundant Ig heavy chains detected in both control individuals and KC patients were Ig α-1 and Ig α-2 likely correlating to the higher IgA levels reported in human tears. We identified significant differences in immunoglobulin κ-chain V-II levels in KC patients compared to control individuals with no significant difference in Ig κ/Ig λ ratios or heavy chain levels. Our study supports previous findings suggesting that KC possesses a systemic component that may contribute to the KC pathology. Further studies are required to define causality and establish a role for systemic immune system-dependent factors and pro-inflammatory processes in KC development or progression. |
format | Online Article Text |
id | pubmed-7287105 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-72871052020-06-15 Characterization of Tear Immunoglobulins in a Small-Cohort of Keratoconus Patients McKay, Tina B. Serjersen, Henrik Hjortdal, Jesper Zieske, James D. Karamichos, Dimitrios Sci Rep Article Keratoconus (KC) is classically considered a non-inflammatory condition caused by central corneal thinning that leads to astigmatism and reduced visual acuity. Previous studies have identified increased systemic levels of pro-inflammatory factors, including interleukin-6, tumor necrosis factor-α, and matrix metalloproteinase-9, suggesting that KC may have an inflammatory component in at least a subset of patients. In this study, we evaluated the levels of different immunoglobulins (light and heavy chains) based on Ig α, Ig λ, Ig κ, Ig µ, and Ig heavy chain subunits in non-KC tears (n = 7 control individuals) and KC tears (n = 7 KC patients) using tandem-liquid chromatography mass spectrometry. The most abundant Ig heavy chains detected in both control individuals and KC patients were Ig α-1 and Ig α-2 likely correlating to the higher IgA levels reported in human tears. We identified significant differences in immunoglobulin κ-chain V-II levels in KC patients compared to control individuals with no significant difference in Ig κ/Ig λ ratios or heavy chain levels. Our study supports previous findings suggesting that KC possesses a systemic component that may contribute to the KC pathology. Further studies are required to define causality and establish a role for systemic immune system-dependent factors and pro-inflammatory processes in KC development or progression. Nature Publishing Group UK 2020-06-10 /pmc/articles/PMC7287105/ /pubmed/32523038 http://dx.doi.org/10.1038/s41598-020-66442-7 Text en © The Author(s) 2020 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 McKay, Tina B. Serjersen, Henrik Hjortdal, Jesper Zieske, James D. Karamichos, Dimitrios Characterization of Tear Immunoglobulins in a Small-Cohort of Keratoconus Patients |
title | Characterization of Tear Immunoglobulins in a Small-Cohort of Keratoconus Patients |
title_full | Characterization of Tear Immunoglobulins in a Small-Cohort of Keratoconus Patients |
title_fullStr | Characterization of Tear Immunoglobulins in a Small-Cohort of Keratoconus Patients |
title_full_unstemmed | Characterization of Tear Immunoglobulins in a Small-Cohort of Keratoconus Patients |
title_short | Characterization of Tear Immunoglobulins in a Small-Cohort of Keratoconus Patients |
title_sort | characterization of tear immunoglobulins in a small-cohort of keratoconus patients |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7287105/ https://www.ncbi.nlm.nih.gov/pubmed/32523038 http://dx.doi.org/10.1038/s41598-020-66442-7 |
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