June 2015
Volume 56, Issue 7
ARVO Annual Meeting Abstract  |   June 2015
Mechanisms of V-domain Ig suppressor of T cell activation (VISTA)-mediated acceptance of corneal allografts
Author Affiliations & Notes
  • Tomoyuki Kunishige
    Nippon Medical School, Tokyo, Japan
  • Hiroko Taniguchi
    Nippon Medical School, Tokyo, Japan
  • Tatsukuni Ohno
    Tokyo Medical and Dental University, Tokyo, Japan
  • Miyuki Azuma
    Tokyo Medical and Dental University, Tokyo, Japan
  • Junko Hori
    Nippon Medical School, Tokyo, Japan
  • Footnotes
    Commercial Relationships Tomoyuki Kunishige, None; Hiroko Taniguchi, None; Tatsukuni Ohno, None; Miyuki Azuma, None; Junko Hori, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 4872. doi:
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      Tomoyuki Kunishige, Hiroko Taniguchi, Tatsukuni Ohno, Miyuki Azuma, Junko Hori; Mechanisms of V-domain Ig suppressor of T cell activation (VISTA)-mediated acceptance of corneal allografts. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4872.

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

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Purpose: V-domain Ig suppressor of T cell activation (VISTA) is a novel and structurally distinct Ig superfamily inhibitory ligand. We have previously demonstrated that survival of allografts treated with anti-VISTA mAb was less than that of the control, and that VISTA plays important role in induction of alloantigen-specific ACAID. (1) To further investigate the mechanism of VISTA-mediated corneal allograft survival, we examined destruction of corneal endothelial cells (CECs) by allo-reactive T cells in vitro. (2) As the next, we examined infiltrating T cells in the graft-bearing eyes from the recipients treated with anti-VISTA or control IgG.

Methods: The corneas from C57BL/6 (B6) eyes pre-treated with anti-VISTA mAb or control rat IgG were incubated with CD4+ T cells for 6h. Dead CECs stained with propidium iodide were counted and compared. (2) Normal corneas of C57BL/6 were transplanted into normal eyes of BALB/c mice. Recipients were administrated with 0.2 mg of anti-VISTA mAb or control rat IgG, three times a week after grafting. For Immunohistochemical staining, graft-bearing eyes were removed.

Results: No significant differences were observed between the number of dead CECs treated with anti-VISTA monoclonal antibodies (mAb) and that treated with control IgG after incubation with allo-reactive T cells. It is indicated that VISTA does not have protective effect in the cornea from the allo-specific killing by CD4 T cells. (2) Immunofluorescent staining of the graft-bearing eyes at 3 to 5 weeks after grafting revealed that the number of infiltrating CD4+ T cells and CD8+ T cells at graft center and host-graft junction were significantly higher in anti-VISTA treated recipients compared to control.

Conclusions: Taken together of our present and previous data, it is suggested that VISTA plays an role in the acceptance of corneal allografts by inducing allo-specific ACAID which suppress T cell infiltration into the cornea, although VISTA doesn’t have a local protective effect in the interaction between CECs and CD4+ T cells.


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