Objective:

To investigate the role of CCL25 in ocular immunity during herpes simplex virus type 1 (HSV-1) infection and its implications for the gut-eye axis.

Approach:

• Experimental Design: Utilized CCL25-deficient (CCL25(–/–)) mice and wild-type C57BL/6J controls infected ocularly with HSV-1 to assess corneal disease severity, viral replication, and survival.
• Immunological Assessment: Analyzed the presence of antiviral effector memory CD4+ and CD8+ T cells in various tissues and measured mucosal chemokine expression.

Key Findings:

• CCL25 deficiency resulted in more severe corneal disease and increased viral replication in CCL25(–/–) mice compared to wild-type controls.
• CCL25(–/–) mice exhibited reduced survival rates compared to wild-type controls.
• Fewer antiviral effector memory CD44+CD4+ and CD44+CD8+ T cells were found in CCL25(–/–) mice across various tissues.
• Activated tissue-resident CD69+CD103+CD4+ and CD69+CD103+CD8+ TRM cells producing interferon-γ were also reduced in CCL25(–/–) mice.
• Strong CCL25 expression was observed in the gut, while it was absent in the cornea or conjunctiva.

Interpretation:

CCL25 is implicated in the recruitment of antiviral effector memory T cells to the cornea during HSV-1 infection, contributing to the understanding of the gut-eye axis in herpes immunity.

Limitations:

• The study primarily focused on CCL25's role without exploring other potential pathways or chemokines involved in ocular immunity.
• Findings are based on mouse models, which may not fully translate to human ocular herpes immunity.

Conclusion:

The findings suggest that the CCL25/CCR9 pathway may be relevant for future research into protective strategies against herpetic eye disease.