CCL25 chemokine promotes antiviral tissue resident CD4+ and CD8+ effector memory TRM cells associated with a reduction of ocular herpes infection and disease: a potential gut–eye axis in herpes immunity - Report - MDSpire

CCL25 chemokine promotes antiviral tissue resident CD4+ and CD8+ effector memory TRM cells associated with a reduction of ocular herpes infection and disease: a potential gut–eye axis in herpes immunity

  • By

  • Azizur Rahman

  • Swayam Prakash

  • Sweta Karan

  • Sarah Xue Le Ng

  • Gina Park

  • Chhaya Maurya

  • America Garcia

  • Khan Intharachalit

  • Junseong Hwang

  • Celine Tze Yao Tang

  • Reilly Andrew Chow

  • Baverly Sabathini Suoth

  • Emma Jane Liao

  • Lbachir BenMohamed

  • July 17, 2026

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Clinical Report: The Role of CCL25 Chemokine in Ocular Herpes Immunity

Overview

CCL25 deficiency in mice resulted in increased severity of corneal disease and reduced survival following ocular HSV-1 infection. The study highlights the importance of CCL25 in recruiting antiviral effector memory T cells to the cornea.

Background

Herpes simplex virus type 1 (HSV-1) is a leading cause of infectious corneal blindness, with significant annual cases of HSV keratitis. Effective immune responses, particularly the recruitment of CD4+ and CD8+ T cells, are crucial for controlling HSV-1 and preventing recurrent herpetic stromal keratitis. Understanding the mechanisms that enhance ocular immunity is vital for developing targeted therapies.

Data Highlights

FindingCCL25(–/–) MiceWild-Type Mice
Corneal disease severityIncreasedNormal
Viral replicationIncreasedNormal
Survival rateReducedNormal
Antiviral effector memory T cellsFewerMore
Activated TRM cellsReducedNormal

Key Findings

  • CCL25 deficiency led to more severe corneal disease and increased viral replication in HSV-1 infected mice.
  • Fewer antiviral effector memory CD4+ and CD8+ T cells were observed in CCL25(–/–) mice compared to wild-type controls.
  • Activated tissue-resident memory (TRM) cells producing interferon-γ were reduced in CCL25(–/–) mice.
  • CCL25 expression was strong in the gut but absent in the cornea and conjunctiva of wild-type mice.
  • Other mucosal chemokines (CXCL14, CXCL17, CCL28) were upregulated in wild-type mice but remained low in CCL25(–/–) mice.

Clinical Implications

The findings indicate the potential relevance of the CCL25/CCR9 pathway in ocular immunity against HSV-1.

Conclusion

CCL25 is involved in recruiting antiviral T cells to the cornea during HSV-1 infection.

Related Resources & Content

  1. Frontiers | CCL25 Chemokine Promotes Antiviral Tissue Resident CD4⁺ and CD8⁺ Effector Memory TRM cells Associated with a Reduction of Ocular Herpes Infection and Disease: A potential Gut–Eye Axis in Herpes Immunity
  2. Acyclovir for the Prevention of Recurrent Herpes Simplex Virus Eye Disease | New England Journal of Medicine
  3. The immunobiology of corneal HSV-1 infection and herpetic stromal keratitis | Clinical Microbiology Reviews
  4. The Journal of Infectious Diseases — Lack of Toll-Like Receptor 9 Exacerbates Ocular Impairment and Visual Loss During Systemic Cryptococcus gattii Infection
  5. Frontiers in Immunology — α-Galactosylceramide-expanded virtual memory CD8+ T cells confer protection against a broad range of pathogens
  6. Frontiers in Immunology — Limited adaptability of virtual memory CD8 T cells to chronic viral infection
  7. Brain — Insights from EBV-specific T-cell Activity Regarding Multiple Sclerosis
  8. Acyclovir for the Prevention of Recurrent Herpes Simplex Virus Eye Disease | New England Journal of Medicine
  9. The immunobiology of corneal HSV-1 infection and herpetic stromal keratitis | Clinical Microbiology Reviews
  10. Frontiers | CCL25 Chemokine Promotes Antiviral Tissue Resident CD4⁺ and CD8⁺ Effector Memory TRM cells Associated with a Reduction of Ocular Herpes Infection and Disease: A potential Gut–Eye Axis in Herpes Immunity

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