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Involvement of programmed death-ligand 2 (PD-L2) in the development of experimental allergic conjunctivitis in mice
  1. A Fukushima1,
  2. T Yamaguchi1,
  3. M Azuma2,
  4. H Yagita3,
  5. H Ueno1
  1. 1Department of Ophthalmology, Kochi Medical School, Kochi University, Japan
  2. 2Department of Molecular Immunology, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan
  3. 3Department of Immunology, Juntendo University School of Medicine, Japan
  1. Correspondence to: Atsuki Fukushima MD, PhD, Department of Ophthalmology, Kochi Medical School, Kochi University, Kohasu, Oko-cho, Nankoku-city 783-8505, Japan; fukusima{at}med.kochi-u.ac.jp

Abstract

Background/aim: Involvement of programmed death-1 (PD-1) and its ligands has been demonstrated in experimental allergic airway disease. Here, the authors aimed to examine whether PD-1 and its ligands are involved in the development of experimental allergic conjunctivitis (EC) in mice.

Methods: EC was induced in Balb/c mice by active immunisation with short ragweed pollen (RW) in alum. 10 days later (day 10), the mice were challenged with eye drops containing RW. 24 hours after the challenge, conjunctivas, spleens, and sera were harvested for histological analysis, cytokine assays, and measurement of RW specific Ig levels. The actively immunised mice were treated with anti-PD-1, anti-PD-L1, anti-PD-L2 antibodies (Abs), or normal rat immunoglobulin G (nrIgG) during either the induction (day 0, 2, 4, 6, and 8) or the effector (2 hours before RW challenge on day 10) phase.

Results: Ab treatment during the induction phase did not affect eosinophil infiltration although immune responses were modulated. In contrast, treatment with anti-PD-L2 Ab, but not anti-PD-1 or anti-PD-L1 Ab, during the effector phase significantly increased eosinophil infiltration into the conjunctiva without affecting systemic immune responses.

Conclusions: Similar to allergic airway inflammation, PD-L2 is involved in the development of EC during the effector phase but not the induction phase.

  • Abs, antibodies
  • AC, allergic conjunctivitis
  • AKC, atopic keratoconjunctivitis
  • ALP, alkaline phosphatase
  • B7RP-1, B7 related protein 1
  • CTLA, cytotoxic T lymphocyte associated antigen
  • EC, experimental allergic conjunctivitis
  • ICOS, inducible co-stimulator
  • nrIgG, normal rat immunoglobulin G
  • PBS, phosphate buffered saline
  • PD, programmed death
  • PD-L2, programmed death-ligand 2
  • RW, ragweed pollen
  • TNF, tumour necrosis factor
  • VKC, vernal keratoconjunctivitis
  • allergic conjunctivitis
  • mouse
  • programmed death
  • ligands
  • Abs, antibodies
  • AC, allergic conjunctivitis
  • AKC, atopic keratoconjunctivitis
  • ALP, alkaline phosphatase
  • B7RP-1, B7 related protein 1
  • CTLA, cytotoxic T lymphocyte associated antigen
  • EC, experimental allergic conjunctivitis
  • ICOS, inducible co-stimulator
  • nrIgG, normal rat immunoglobulin G
  • PBS, phosphate buffered saline
  • PD, programmed death
  • PD-L2, programmed death-ligand 2
  • RW, ragweed pollen
  • TNF, tumour necrosis factor
  • VKC, vernal keratoconjunctivitis
  • allergic conjunctivitis
  • mouse
  • programmed death
  • ligands

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