Restoration of antitumor immunity through anti-MICA antibodies elicited with a chimeric protein

J Immunother Cancer. 2020 Jun;8(1):e000233. doi: 10.1136/jitc-2019-000233. Epub 2020 Jun 8.

Abstract

Background: Natural killer and cytotoxic CD8+ T cells are major players during antitumor immunity. They express NKG2D, an activating receptor that promotes tumor elimination through recognition of the MHC class I chain-related proteins A and B (MICA and MICB). Both molecules are overexpressed on a great variety of tumors from different tissues, making them attractive targets for immunotherapy. However, tumors shed MICA and MICB, and the soluble forms of both (sMICA and sMICB) mediate tumor-immune escape. Some reports indicate that anti-MICA antibodies (Ab) can promote the restoration of antitumor immunity through the induction of direct antitumor effects (antibody-dependent cell-mediated cytotoxicity, ADCC) and scavenging of sMICA. Therefore, we reasoned that an active induction of anti-MICA Ab with an immunogenic protein might represent a novel therapeutic and prophylactic alternative to restore antitumor immunity.

Methods: We generated a highly immunogenic chimeric protein (BLS-MICA) consisting of human MICA fused to the lumazine synthase from Brucella spp (BLS) and used it to generate anti-MICA polyclonal Ab (pAb) and to investigate if these anti-MICA Ab can reinstate antitumor immunity in mice using two different mouse tumors engineered to express MICA. We also explored the underlying mechanisms of this expected therapeutic effect.

Results: Immunization with BLS-MICA and administration of anti-MICA pAb elicited by BLS-MICA significantly delayed the growth of MICA-expressing mouse tumors but not of control tumors. The therapeutic effect of immunization with BLS-MICA included scavenging of sMICA and the anti-MICA Ab-mediated ADCC, promoting heightened intratumoral M1/proinflammatory macrophage and antigen-experienced CD8+ T cell recruitment.

Conclusions: Immunization with the chimeric protein BLS-MICA constitutes a useful way to actively induce therapeutic anti-MICA pAb that resulted in a reprogramming of the antitumor immune response towards an antitumoral/proinflammatory phenotype. Hence, the BLS-MICA chimeric protein constitutes a novel antitumor vaccine of potential application in patients with MICA-expressing tumors.

Keywords: immunology.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal / pharmacology*
  • Antibody-Dependent Cell Cytotoxicity / immunology*
  • Brucella / enzymology
  • Female
  • Histocompatibility Antigens Class I / genetics
  • Histocompatibility Antigens Class I / immunology*
  • Lymphoma / immunology*
  • Lymphoma / pathology
  • Lymphoma / therapy
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Multienzyme Complexes / genetics
  • Multienzyme Complexes / immunology
  • NK Cell Lectin-Like Receptor Subfamily K / genetics
  • NK Cell Lectin-Like Receptor Subfamily K / immunology
  • Recombinant Fusion Proteins / immunology*
  • Tumor Cells, Cultured
  • Urinary Bladder Neoplasms / immunology*
  • Urinary Bladder Neoplasms / pathology
  • Urinary Bladder Neoplasms / therapy

Substances

  • Antibodies, Monoclonal
  • Histocompatibility Antigens Class I
  • MHC class I-related chain A
  • Multienzyme Complexes
  • NK Cell Lectin-Like Receptor Subfamily K
  • Recombinant Fusion Proteins
  • 6,7-dimethyl-8-ribityllumazine synthase