June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
The Role of Group 2 Innate lymphoid Cells (ILC2s) in Mouse Models of Papain-Induced Conjunctivitis.
Author Affiliations & Notes
  • Jobu Sugita
    Depatrment of Ophthalmology, Juntendo University School of Medicine, Tokyo, Japan
    Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan
  • Akira Matsuda
    Depatrment of Ophthalmology, Juntendo University School of Medicine, Tokyo, Japan
  • Yosuke Asada
    Depatrment of Ophthalmology, Juntendo University School of Medicine, Tokyo, Japan
    Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan
  • Nobuyuki Ebihara
    Department of Ophthalmology, Juntendo Urayasu Hospital, Chiba, Japan
  • Akira Murakami
    Depatrment of Ophthalmology, Juntendo University School of Medicine, Tokyo, Japan
  • Susumu Nakae
    Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan
  • Footnotes
    Commercial Relationships Jobu Sugita, None; Akira Matsuda, None; Yosuke Asada, None; Nobuyuki Ebihara, None; Akira Murakami, None; Susumu Nakae, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 4881. doi:
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      Jobu Sugita, Akira Matsuda, Yosuke Asada, Nobuyuki Ebihara, Akira Murakami, Susumu Nakae; The Role of Group 2 Innate lymphoid Cells (ILC2s) in Mouse Models of Papain-Induced Conjunctivitis.. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4881.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: Group 2 innate lymphoid cells (ILC2s) produce large amounts of Th2 cytokines in response to IL-33 and induce eosinophil infiltration. We previously identified ILC2s in mouse lacrimal glands and in conjunctivae in response to papain induced inflammation. To clarify the role of ILC2s in papain-induced conjunctivitis, ILC2s were depleted in mice models.

Methods: To make papain-induced conjunctivitis model mice, papain-soaked soft contact lens (2mm diameter) was inserted into the conjunctival sacs of C57/BL6 (B6)-Rag2-/- mice. To deplete ILC2s, 200 μg of anti-CD25 antibody was injected into the Rag2-/- mice two days before contact lens insertion. We also used B6-Rag2/common γ chain (cγ)-/-, which lack acquired immune systems and ILC2s. 4 days after contact lens installation, the eyes were subjected to flow cytometry analysis or histological analysis. To identify mouse ILC2s by a flow cytometer, anti-mouse lineage mix antibodies, ST2, CD25, CD127 and CD90.1 antibodies were used to mouse conjunctival tissues from papain-induced conjunctivitis model.

Results: Anti-CD25 antibody injection in Rag2-/- mice accomplished 93% depletion of ILC2s in the conjunctival tissue compared to PBS injection. The numbers of infiltrated eosinophil in papain-induced conjunctivitis models diminished by the anti-CD25 antibody treatment (48 ± 8 versus 14 ± 6.4, mean number of eosinophil ± SD per slides, n = 8, P< 0.05 by Mann-Whitney’s U test). ILC2 deficient Rag2/cγ-/- mice also showed diminished numbers of eosinophil compared to Rag2-/- mice (53 ± 20 versus 8 ± 4, n = 8 , P< 0.05)

Conclusions: ILC2s depletion by anti-CD25 antibody could diminish eosinophil infiltration in papain-induced conjunctivitis model.

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