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Cells
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Ocular Surface and Adnexal Diseases: Molecular Mechanisms and Treatment Progresses
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Ocular Surface and Adnexal Diseases: Molecular Mechanisms and Treatment Progresses

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 30 August 2026 | Viewed by 2538

Special Issue Editor

Prof. Dr. Edit Tóth-Molnár

E-Mail Website
Guest Editor
Department of Ophtalmology, Albert Szent-Györgyi Health Centre, University of Szeged, Korányi Fasor 10-11, H-6720 Szeged, Hungary
Interests: dry eye disease; tear biomarkers; eyelid diseases; lacrimal gland diseases; molecular mechanisms

Special Issue Information

Dear Colleagues,

We are pleased to announce a forthcoming Cells Special Issue titled “Ocular Surface and Adnexal Diseases: Molecular Mechanisms and Treatment Progresses”. This issue will serve as a comprehensive platform for research dedicated to exploring the cellular and molecular mechanisms underlying ocular surface, eyelid, and lacrimal gland diseases, alongside highlighting cutting-edge developments in clinical strategies for their treatment.

Ocular surface and adnexal diseases—including dry eye disease, blepharitis, meibomian gland dysfunction, conjunctivitis, lacrimal gland diseases, and corneal disorders—affect millions worldwide and significantly impair visual function and quality of life. Recent years have witnessed considerable progress in our understanding of the pathogenesis of these conditions, encompassing inflammatory signaling pathways, epithelial barrier dysfunction, immune cell dynamics, microbiome alterations, and neurogenic mechanisms. Simultaneously, novel therapeutic strategies, ranging from biologics to regenerative approaches, are being developed and evaluated.

This Special Issue invites contributions that explore, but are not limited to, the following topics:

  • Cellular and molecular mechanisms underlying ocular surface inflammation and degeneration;
  • Role of immune cells and cytokines in disease progression;
  • Epithelial–mesenchymal interactions and wound healing;
  • Pathomechanisms of eyelid diseases;
  • New treatment options for eyelid diseases;
  • Advances in diagnostics and molecular biomarkers;
  • Impact of microbiota on ocular surface health and disease;
  • Preclinical and clinical studies of emerging therapeutic approaches;
  • Gene- and cell-based therapies for ocular surface regeneration;
  • Drug delivery systems targeting the ocular surface.

Both original research articles and high-quality reviews are welcome. Contributions should provide new insights or critical syntheses that advance the understanding of ocular surface/adnexal diseases and/or improve patient outcomes through innovative treatments.

Prof. Dr. Edit Tóth-Molnár
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • ocular surface and adnexal diseases
  • dry eye disease
  • eyelid diseases
  • lacrimal gland diseases
  • molecular mechanisms
  • therapeutic strategies

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (4 papers)

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Research

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18 pages, 4829 KB  
Article
Patient-Derived Immortalized Limbal Epithelial Cells as In Vitro Models of Congenital Aniridia
by Tanja Stachon, Shweta Suiwal, Virendra Kumar, Tobias May, Frank Schmitz, Maryam Amini, Fabian N. Fries, Berthold Seitz, Shao-Lun Hsu, Shuailin Li, Shanhe Liu, Swarnali Kundu, Nicole Ludwig and Nóra Szentmáry
Cells 2026, 15(5), 394; https://doi.org/10.3390/cells15050394 - 24 Feb 2026
Viewed by 402
Abstract
Purpose: To establish and comprehensively characterize immortalized limbal epithelial cell lines derived from patients with PAX6 haploinsufficiency-associated congenital aniridia, as well as from a healthy donor. These well-defined cell models provide a reliable and reproducible platform for long-term experimental studies, facilitating mechanistic investigations [...] Read more.
Purpose: To establish and comprehensively characterize immortalized limbal epithelial cell lines derived from patients with PAX6 haploinsufficiency-associated congenital aniridia, as well as from a healthy donor. These well-defined cell models provide a reliable and reproducible platform for long-term experimental studies, facilitating mechanistic investigations and the development and evaluation of novel therapeutic approaches. Methods: Primary limbal epithelial cells were isolated from biopsies of two patients with distinct PAX6 variants and from a healthy donor. Immortalization was performed by InSCREENex GmbH. The resulting cell lines were characterized using microscopy, BrdU assay, qPCR, flow cytometry, immunocytochemistry, and mRNA sequencing. Results: Immortalized aniridia and control cell lines displayed typical polygonal epithelial morphology and comparable proliferation rates. Total PAX6 mRNA and protein levels were similar among groups; however, nuclear PAX6 immunosignals were significantly reduced in aniridia-derived lines. Expression of ABCG2, TP63, FOSL2, ALDH1A1, and FABP5 showed no significant differences, except for reduced ΔNp63α protein levels in one aniridia line. mRNA sequencing detected more than 14,000 transcripts, including subsets uniquely expressed in control and aniridia-derived lines. Conclusions: Immortalized aniridia limbal epithelial cell lines preserve key epithelial characteristics and overall transcriptomic similarity to controls while exhibiting disease-relevant molecular alterations. These cell lines represent models of PAX6-associated ocular surface disease. Full article
(This article belongs to the Special Issue Ocular Surface and Adnexal Diseases: Molecular Mechanisms and Treatment Progresses)
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20 pages, 7802 KB  
Article
mRNA Sequencing of Limbal Epithelial Cells and mRNA/miRNA Profiling of Limbal Stromal Cells in PAX6-Related Congenital Aniridia
by Tanja Stachon, Shweta Suiwal, Maryam Amini, Marta Corton, Fabian Norbert Fries, Berthold Seitz, Nicole Ludwig, Shusruto Rishik, Andreas Keller and Nóra Szentmáry
Cells 2026, 15(4), 340; https://doi.org/10.3390/cells15040340 - 13 Feb 2026
Viewed by 513
Abstract
The dysfunction of limbal epithelial cells (LECs) and limbal stromal cells (LSCs) in congenital aniridia remains incompletely understood. We aimed to analyze mRNA expression profiles of primary human LECs and LSCs, as well as microRNA (miRNA) expression in LSCs, from patients with congenital [...] Read more.
The dysfunction of limbal epithelial cells (LECs) and limbal stromal cells (LSCs) in congenital aniridia remains incompletely understood. We aimed to analyze mRNA expression profiles of primary human LECs and LSCs, as well as microRNA (miRNA) expression in LSCs, from patients with congenital aniridia (AN-LECs and AN-LSCs). mRNA sequencing of primary human LECs and mRNA and miRNA sequencing of LSCs were performed from patients with aniridia and healthy controls. Gene ontology and pathway analyses were used to evaluate biological processes, cellular components, and molecular functions. Selected deregulated mRNAs and miRNAs were validated by quantitative real-time PCR (RT-qPCR). A total of 188 differentially expressed genes (DEGs) were identified in AN-LECs, and 3001 DEGs in AN-LSCs. In AN-LECs, the top hub genes were associated with inflammatory and interferon-related responses. In contrast, AN-LSCs showed predominant deregulation of mitochondrial and metabolic genes. Pathway analysis revealed involvement of inflammation-related pathways in AN-LECs and metabolic pathways in AN-LSCs. Additionally, 48 deregulated miRNAs were identified in AN-LSCs. This study provides comprehensive mRNA profiles of LECs and LSCs and miRNA profiles of LSCs in congenital aniridia. The findings emphasize the importance of LSC influence and offer insights into molecular mechanisms underlying aniridia-associated keratopathy (AAK), supporting future research and potential therapeutic target identification. Full article
(This article belongs to the Special Issue Ocular Surface and Adnexal Diseases: Molecular Mechanisms and Treatment Progresses)
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Review

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17 pages, 941 KB  
Review
Molecular and Cellular Effects of Therapies for Thyroid Eye Disease on Ocular Surface and Adnexal Homeostasis
by Monika Sarnat-Kucharczyk, Wojciech Luboń, Dorota Wyględowska-Promieńska and Adrian Smędowski
Cells 2026, 15(7), 622; https://doi.org/10.3390/cells15070622 - 31 Mar 2026
Viewed by 431
Abstract
Thyroid eye disease (TED) is an autoimmune inflammatory disorder primarily affecting orbital tissues, but ocular surface and adnexal involvement represent a frequent and clinically significant component of disease burden. Beyond mechanical exposure resulting from eyelid retraction and proptosis, TED-associated ocular surface disease arises [...] Read more.
Thyroid eye disease (TED) is an autoimmune inflammatory disorder primarily affecting orbital tissues, but ocular surface and adnexal involvement represent a frequent and clinically significant component of disease burden. Beyond mechanical exposure resulting from eyelid retraction and proptosis, TED-associated ocular surface disease arises from complex interactions between immune activation, epithelial stress, glandular dysfunction, and altered neuro-epithelial signaling. Increasing use of systemic immunomodulatory therapies, biologics, and orbital radiotherapy has improved control of orbital inflammation; however, their molecular and cellular effects on ocular surface homeostasis remain incompletely defined. This review summarizes current evidence on the cellular and molecular mechanisms underlying ocular surface dysfunction in TED and examines how disease-modifying therapies influence epithelial integrity, tear film stability, meibomian and lacrimal gland function, and local immune signaling. Key pathways discussed include cytokine-mediated inflammation, thyroid-stimulating hormone receptor and insulin-like growth factor-1 receptor crosstalk, pro-fibrotic signaling, neuro-inflammatory mechanisms, and epithelial stress responses involving mitogen-activated protein kinase and nuclear factor kappa B pathways. We further highlight the challenge of disentangling therapy-induced molecular effects from persistent exposure-related mechanical stress. Understanding how TED therapies modulate ocular surface and adnexal homeostasis is essential for optimizing integrated management strategies that address both orbital inflammation and long-term ocular surface stability. Full article
(This article belongs to the Special Issue Ocular Surface and Adnexal Diseases: Molecular Mechanisms and Treatment Progresses)
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24 pages, 385 KB  
Review
Autoimmune Ocular Surface Disorders: From Molecular Immunopathogenesis to Regenerative and Surgical Therapeutics
by Wojciech Luboń, Marta Świerczyńska, Katarzyna Jadczyk-Sorek and Dorota Wyględowska-Promieńska
Cells 2026, 15(4), 378; https://doi.org/10.3390/cells15040378 - 22 Feb 2026
Viewed by 687
Abstract
Autoimmune ocular surface diseases represent a complex group of disorders in which systemic immune dysregulation triggers chronic inflammation, epithelial dysfunction, and progressive tissue fibrosis. Systemic lupus erythematosus, primary Sjögren’s syndrome, and ocular cicatricial pemphigoid are the principal entities linking systemic autoimmunity to ocular [...] Read more.
Autoimmune ocular surface diseases represent a complex group of disorders in which systemic immune dysregulation triggers chronic inflammation, epithelial dysfunction, and progressive tissue fibrosis. Systemic lupus erythematosus, primary Sjögren’s syndrome, and ocular cicatricial pemphigoid are the principal entities linking systemic autoimmunity to ocular surface pathology. These conditions share convergent mechanisms—including dysregulated cytokine signaling (IFN-I, IL-6, and IL-17), complement activation, and epithelial–mesenchymal transition—culminating in tear film instability and visual impairment. Recent advances in molecular immunology and omics profiling have elucidated disease-specific pathways and identified actionable therapeutic targets. Conventional immunosuppressants such as corticosteroids and cyclosporine remain fundamental, yet emerging biologics targeting BAFF, IFNAR, and JAK/STAT signaling—alongside regenerative strategies employing mesenchymal and induced pluripotent stem cells—are transforming disease management. Parallel innovations in amniotic membrane transplantation, keratoprosthesis, and bioengineered corneal scaffolds integrate structural reconstruction with immune modulation. Furthermore, the convergence of multi-omics analytics, artificial intelligence-assisted diagnostics, and microbiome-based immunomodulation heralds a new era of precision ophthalmology. This review synthesizes current molecular insights, clinical observations, and translational advances that collectively redefine autoimmune ocular surface diseases—from chronic inflammatory disorders into a targetable, regenerative, and potentially reversible spectrum of conditions. Full article
(This article belongs to the Special Issue Ocular Surface and Adnexal Diseases: Molecular Mechanisms and Treatment Progresses)
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