Characterization of neutralizing antibodies reacting with the 213-224 amino-acid segment of human galectin-9

PLoS One. 2018 Sep 11;13(9):e0202512. doi: 10.1371/journal.pone.0202512. eCollection 2018.

Abstract

Extra-cellular galectin-9 (gal-9) is an immuno-modulatory protein with predominant immunosuppressive effects. Inappropriate production of gal-9 has been reported in several human malignancies and viral diseases like nasopharyngeal, pancreatic and renal carcinomas, metastatic melanomas and chronic active viral hepatitis. Therefore therapeutic antibodies neutralizing extra-cellular gal-9 are expected to contribute to immune restoration in these pathological conditions. Two novel monoclonal antibodies targeting gal-9 -Gal-Nab 1 and 2-have been produced and characterized in this study. We report a protective effect of Gal-Nab1 and Gal-Nab2 on the apoptotic cell death induced by gal-9 in primary T cells. In addition, they inhibit late phenotypic changes observed in peripheral T cells that survive gal-9-induced apoptosis. Gal-Nab1 and Gal-Nab2 bind nearly identical, overlapping linear epitopes contained in the 213-224 amino-acid segments of gal-9. Nevertheless, they have some distinct functional characteristics suggesting that their three-dimensional epitopes are distinct. These differences are best demonstrated when gal-9 is applied on Jurkat cells where Gal-Nab1 is less efficient than Gal-Nab2 in the prevention of apoptotic cell death. In addition, Gal-Nab1 stimulates non-lethal phosphatidylserine translocation at the plasma membrane and calcium mobilization triggered by gal-9 in these cells. Both Gal-Nab1 and 2 cross-react with murine gal-9. They bind its natural as well as its recombinant form. This cross-species recognition will be an advantage for their assessment in pre-clinical tumor models.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal / pharmacology*
  • Antibodies, Neutralizing / pharmacology*
  • Apoptosis / drug effects
  • Biological Transport
  • Calcium / metabolism
  • Epitopes / immunology*
  • Galectins / adverse effects
  • Galectins / chemistry*
  • Galectins / immunology
  • Humans
  • Immunization
  • Jurkat Cells
  • Mice
  • Phosphatidylserines / metabolism
  • T-Lymphocytes / cytology*
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / metabolism

Substances

  • Antibodies, Monoclonal
  • Antibodies, Neutralizing
  • Epitopes
  • Galectins
  • LGALS9 protein, human
  • Phosphatidylserines
  • Calcium

Grants and funding

This work was supported by Idex Saclay - Satt Saclay, Prematuration Grant 2015, https://www.satt-paris-saclay.fr/; BMS Foundation for Immuno-Oncology- Grant 2016-2017, http://fondation-bms.fr/. Several authors were employed by commercial companies: Cellvax (CL, CB, MW), GalPharma Co, Ltd (TN), H-Immune Therapeutics (LC). These companies provided support in the form of salaries for authors [CL, CB, MW, TN, LC], but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific roles of these authors are articulated in the ‘author contributions’ section.