July 2019
Volume 60, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2019
High content imaging assay for detection of immunological synapse inhibition of ICAM-1/LFA-1 binding with lifitegrast
Author Affiliations & Notes
  • Anneli Savinainen
    Shire, Lexington, Massachusetts, United States
  • Anthony Essex
    PhenoVista Biosciences, San Diego, California, United States
  • Galen Carey
    Shire, Lexington, Massachusetts, United States
  • Geoff Grandjean
    PhenoVista Biosciences, San Diego, California, United States
  • Footnotes
    Commercial Relationships   Anneli Savinainen, Shire (E); Anthony Essex, PhenoVista Biosciences (E), Shire (C); Galen Carey, Shire (E); Geoff Grandjean, PhenoVista Biosciences (E), Shire (C)
  • Footnotes
    Support  This study was funded by Shire.
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 286. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Anneli Savinainen, Anthony Essex, Galen Carey, Geoff Grandjean; High content imaging assay for detection of immunological synapse inhibition of ICAM-1/LFA-1 binding with lifitegrast. Invest. Ophthalmol. Vis. Sci. 2019;60(9):286.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose : Interaction between the adhesion molecules ICAM-1 and LFA-1 on dendritic cells and T cells, respectively, is believed to mediate immunological synapse (IS) formation. ICAM-1 is overexpressed in dry eye disease (DED) and is a key factor in the development of ocular surface inflammation. Lifitegrast ophthalmic solution 5% is an LFA-1 antagonist indicated for the treatment of the signs and symptoms of DED. A high content imaging assay was developed to verify that lifitegrast prevents the ligand interaction between ICAM-1 and LFA-1 within the IS.

Methods : Cultures of human CD4+ T-cells in the presence of either activated (with LPS or IFNgamma) or non-activated normal primary human dendritic cells were plated in 384-well plates and exposed to either lifitegrast, efalizumab (an anti-LFA-1 antibody, control), or compound 4 (lifitegrast analog, positive control) at increasing concentrations. Antibodies against ICAM-1 and LFA-1 were used to detect IS by wide-field fluorescence imaging. Positive IS formation (synapse count) was defined by regions of ICAM-1 and LFA-1 accumulation and proximity to nearest ICAM-1 or LFA-1 positive neighbour (cells not proximal to other positive cells were omitted). Half maximal inhibitory concentration (IC50) values were separately calculated for LFA-1 and ICAM-1 positive cells.

Results : In activated cells, inhibition of IS formation with lifitegrast (IC50 of LFA-1, 1.781 µM and ICAM-1, 3.842 µM) or the lifitegrast analog (IC50 of LFA-1, 0.043 µM and ICAM-1, 0.136 µM) was more potent than with efalizumab (Figure).

Conclusions : Lifitegrast displayed potent concentration-dependent prevention of IS formation between ICAM-1 and LFA-1 in a robust high-content imaging assay. This interaction is important for downstream T-cell activation and is a key factor in the pathophysiology of DED. The rapid clinical effect of lifitegrast observed in efficacy trials may be attributable to this dose-dependent inhibition of IS formation.

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.

 

Figure. Synapse formation between activated dendritic cells and T-cells

Figure. Synapse formation between activated dendritic cells and T-cells

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×