Immunohistochemical studies in equine recurrent uveitis (ERU).

The study investigates the role of T-cells and B-cells, along with major histocompatibility complex (MHC) class II, in causing the inflammatory eye condition, equine recurrent uveitis (ERU). The study found a high percentage of these cells in the affected horse eyes, suggesting a cell-mediated immune response may be key in causing ERU. It also noted aberrant MHC class II expression in resident ocular cells, indicating abnormal immune regulation could also be a factor.

Research Context

• Equine Recurrent Uveitis (ERU) is an inflammatory eye condition in horses whose cause is not completely understood. The study goals were to investigate the presence and role of T-cells, B cells and major histocompatibility complex (MHC) class II in ERU to gain a better understanding of its pathogenesis.
• In human cases of uveitis, an immunologic driven etiology was established, hinting at a similar cause in ERU. The research explores this possibility by evaluating the presence and role of the immune cells and molecules in the horses afflicted with the condition.

Research Methodology

• The study utilized immunohistochemistry, a process that allows the visualization of cells in tissue using antibodies that bind to specific proteins in the cells. The research focused on markers for T and B lymphocytes (types of white blood cells) and MHC class II antibodies (proteins involved in immune response).
• The study consisted of 20 eyes from 15 horses with ERU, and 26 eyes from 20 horses were used to investigate normal MHC class II expression. Additionally, the number of T-cells in the inflammatory cell population was also studied in 18 eyes from 14 horses.

Research Findings

• The majority of the inflammatory cells in the uvea of the eyes studied were T-cells. Out of the 16 out of 18 eyes studied (89%), the T-cell population was more than 70%. B lymphocytes were present within the centre of follicular aggregates in three eyes.
• The high percentage of T-cells, suggests that cell-mediated immune response is a central factor in ERU etiology.
• An increase in MHC class II expression was observed in the trabecular meshwork and on the nonpigmented ciliary epithelium, as well as aberrant MHC class II expressions on proliferating Müller cells and retinal pigment epithelial cells.
• The unusual expression of MHC class II on resident ocular cells, might demonstrate that abnormal immune regulation is also implicated in the pathogenesis of ERU.

Conclusions

• The study indicated that cell-mediated immune response, facilitated by T-cells, likely plays a crucial role in ERU pathogenesis. The abnormal propagation of MHC class II on ocular resident cells also suggests that ERU could be triggered or exacerbated due to aberrant immune regulation.