June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
CXCL 12 is a chemoattract induced by HMGB1 in T cell induced uveitis (tEAU)
Author Affiliations & Notes
  • Guomin Jiang
    Department of Ophthalmology, University of Louisville, Louisville, KY
  • Yunsong Wang
    Department of Ophthalmology, Gongren Hospital, Tangshan, China
  • Yuan Zhao
    Department of Pharmaceutical Sciences, Sullivan University College of Pharmacy, Louisville, KY
  • Amir Reza Hajrasouliha
    Department of Ophthalmology, University of Louisville, Louisville, KY
  • Jinhui Wu
    Ophthalmology, Changhai Hospital, Shanghai, China
  • Deming Sun
    Doheny Eye Institute, Los Angeles, CA
  • Henry J Kaplan
    Department of Ophthalmology, University of Louisville, Louisville, KY
  • Hui Shao
    Department of Ophthalmology, University of Louisville, Louisville, KY
  • Footnotes
    Commercial Relationships Guomin Jiang, None; Yunsong Wang, None; Yuan Zhao, None; Amir Reza Hajrasouliha, None; Jinhui Wu, None; Deming Sun, None; Henry Kaplan, None; Hui Shao, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 876. doi:
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      Guomin Jiang, Yunsong Wang, Yuan Zhao, Amir Reza Hajrasouliha, Jinhui Wu, Deming Sun, Henry J Kaplan, Hui Shao; CXCL 12 is a chemoattract induced by HMGB1 in T cell induced uveitis (tEAU). Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):876.

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

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Abstract

Purpose: In EAU induced by injection of uveitogenic, interphotoreceptor retinoid-binding protein (IRBP)-specific T cells (tEAU) in mice, we have previously reported that high mobility group box 1 (HMGB1), an important endogenous danger signal, was an early and critical mediator for induction of disease. Our current study explores the role of HMGB1 in intraocular inflammation, focusing on its role in recruiting infiltrating cells into the eye.

Methods: Supernatants collected from the co-culture of retinal explants with HMGB1 or IRBP-specific T cells in the presence or absence of anti-HMGB1 Ab were tested for their chemoattractive effect on leukocytes. Mice receiving IRBP-specific T cells were treated with CXCR4 antagonist (AMD3100), and intraocular inflammation was examined by funduscopy and histology.

Results: HMGB1 alone or culture supernatants from retinal explants did not attract leukocytes. However, supernatants from retinal explants treated with HMGB1 or co-cultured with IRBP-specific T cells did attract lymphocytes; co-culture in the presence of anti-HMGB1 Ab abrogated chemoattraction, implying molecules released by HMGB1 treated retinal cells are chemoattractive. Moreover, supernatants neutralized by anti-CXCL12 Ab or leukocytes pre-treated with AMD3100 (an antagonist of CXCR4, a receptor for CXCL12) resulted in decreased chemoattraction. Finally, tEAU was significantly inhibited by AMD3100.

Conclusions: CXCL12, a ligand for CXCR4, is produced by retinal cells after exposure to HMGB1 and is a chemoattract for lymphocytes in tEAU.

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