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Cellular Infiltrate in Rheumatoid Arthritis-associated Paracentral Corneal Ulceration
Carolyn M Kalsow1, Steven S S T Ching1, Ronald D Plotnik1
1a Department of Ophthalmology , University of Rochester School of Medicine and Dentistry , Rochester , New York , USA.
Insights
Rheumatoid arthritis can cause rare corneal melting. This study found T-lymphocytes in affected corneal tissue, suggesting an immune system cause for rheumatoid arthritis-associated corneal ulcers.
Area of Science:
- Ophthalmology
- Immunology
- Rheumatology
Background:
- Rheumatoid arthritis is a systemic autoimmune disease.
- Corneal ulceration can be a rare but serious ocular complication.
- Understanding the immunopathogenesis is crucial for effective treatment.
Observation:
- The study analyzed corneal tissues from patients with rheumatoid arthritis-associated central or paracentral corneal ulceration.
- Immunohistochemistry was used to identify infiltrating cells in ulcerated areas.
- Ulcers presented as non-infiltrated lesions with minimal ocular inflammation.
Findings:
- Sparse T-lymphocytes were consistently found in subepithelial areas adjacent to the ulcer.
- Neutrophils and macrophages were present in the corneal stroma.
- B-lymphocytes were not detected, and MHC Class II antigen reactivity was observed on some infiltrating cells and corneal endothelium.
Implications:
- The findings support an immune-mediated pathogenesis for rheumatoid arthritis-associated corneal ulceration.
- Identifying T-lymphocyte infiltration aids in understanding this infrequent corneal melting.
- This research may inform future diagnostic and therapeutic strategies for ocular manifestations of rheumatoid arthritis.
Purpose:
To investigate an immunopathogenesis of central and paracentral corneal ulceration associated with rheumatoid arthritis.
Methods:
Sparse infiltrating cells in the ulcer area were identified by immunohistochemistry applied to archived formalin fixed, paraffin embedded tissues that had been recovered from patients undergoing penetrating keratoplasty necessitated by rheumatoid-associated central or paracentral corneal ulceration.
Results:
Clinically, the ulcers presented as non-infiltrated lesions with a modicum of other ocular inflammation. Sparse T-lymphocytes were consistently identified in the subepithelial areas adjacent to the ulcer, with some neutrophils and macrophages in the stroma. B-lymphocytes were not detected. MHC Class II antigens reactivity was noted on some infiltrating cells and on corneal endothelium of two specimens.
Conclusions:
Immunohistochemistry of archival tissue facilitated detection and identification of sparse infiltrate in this infrequent corneal melting. Selective, consistent finding of T-lymphocyte infiltration in the ulcer area supports an immunopathogenesis of this clinical entity.
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