May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
The Effect of HSV–1–Infected Keratocytes on T Cell Infiltration into Corneal Stroma
Author Affiliations & Notes
  • B.S. Kwon
    Ophthalmology, LSU Eye Ctr, New Orleans, LA
  • H.Y. Park
    Ophthalmology, LSU Eye Ctr, New Orleans, LA
  • Y.H. Kim
    Ophthalmology, LSU Eye Ctr, New Orleans, LA
  • J.H. Choi
    Ophthalmology, LSU Eye Ctr, New Orleans, LA
  • W.J. Kang
    Ophthalmology, LSU Eye Ctr, New Orleans, LA
  • C.H. Kim
    Ophthalmology, LSU Eye Ctr, New Orleans, LA
  • S.K. Lee
    Ophthalmology, LSU Eye Ctr, New Orleans, LA
  • S.K. Seo
    Ophthalmology, LSU Eye Ctr, New Orleans, LA
  • Footnotes
    Commercial Relationships  B.S. Kwon, None; H.Y. Park, None; Y.H. Kim, None; J.H. Choi, None; W.J. Kang, None; C.H. Kim, None; S.K. Lee, None; S.K. Seo, None.
  • Footnotes
    Support  NIH Grant EY013325, EY02377, RPB
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 1650. doi:
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      B.S. Kwon, H.Y. Park, Y.H. Kim, J.H. Choi, W.J. Kang, C.H. Kim, S.K. Lee, S.K. Seo; The Effect of HSV–1–Infected Keratocytes on T Cell Infiltration into Corneal Stroma . Invest. Ophthalmol. Vis. Sci. 2004;45(13):1650.

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

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Abstract

Abstract: : Purpose: Herpetic stromal keratitis (HSK) is an inflammatory disorder induced by HSV–1 infection and characterized by CD4+ T cell–dependent destruction of the corneal stroma. It is not known what triggers CD4+ T cell migration into the corneal stroma following HSV–1 infection. The keratocyte is a fibroblast–like cell and can function as an antigen–presenting cell in the mouse cornea. Keratocytes show an enhanced expression of MHC class II by IFN–γ stimulation and constitutive expression of the costimulatory molecules, B7–1, CD40, and 4–1BBL. We hypothesize that chemokines produced by stromal keratocytes play a role in CD4+ T cell infiltration into the corneal stroma. To test this hypothesis, we examined whether HSV–1–infected keratocytes secreted chemokines and whether T cells that migrated into the cornea carried the appropriate receptors for these chemokines. Methods: Primary cultures of murine stromal keratocytes were infected with HSV–1. Cytokine expression in the keratocytes was determined by both RNA protection assays and ELISA. FACS analysis was used to detect the chemokine receptors on CD4 T cells in the draining lymph nodes. Results: HSV–1–infected keratocytes induced mRNA for RANTES, macrophage–inflammatory protein (MIP)–1ß, MIP–1α, MIP–2, INF–γ–inducible protein (IP)–10, monocyte chemoattractant protein (MCP)–1, and T cell activation (TCA)–3. Uninfected keratocytes showed only a low level of RANTES mRNA. T cells that had infiltrated into the corneal stroma carried mRNA for the chemokine receptors CCR1, CCR2, and CCR5. In in vitro transwell migration assays, the culture supernatant of HSV–1–infected keratocytes vigorously chemoattracted HSV–1–primed T cells, but not unprimed T cells. The migratory capacity of the primed T cells was specific to CCR5, as shown by severely reduced T cell migration with the use of desensitized CCR5. Conclusions: The results suggest that HSV–1–infected keratocytes play a potential role in attracting HSV–1–specific T cells into the corneal stroma.

Keywords: herpes simplex virus • immunomodulation/immunoregulation • cornea: basic science 
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