Critical role of kinase activity of hematopoietic progenitor kinase 1 in anti-tumor immune surveillance

PLoS One. 2019 Mar 26;14(3):e0212670. doi: 10.1371/journal.pone.0212670. eCollection 2019.

Abstract

Immunotherapy has fundamentally changed the landscape of cancer treatment. Despite the encouraging results with the checkpoint modulators, response rates vary widely across tumor types, with a majority of patients exhibiting either primary resistance without a significant initial response to treatment or acquired resistance with subsequent disease progression. Hematopoietic progenitor kinase 1 (HPK1) is predominantly expressed in hematopoietic cell linages and serves as a negative regulator in T cells and dendritic cells (DC). While HPK1 gene knockout (KO) studies suggest its role in anti-tumor immune responses, the involvement of kinase activity and thereof its therapeutic potential remain unknown. To investigate the potential of pharmacological intervention using inhibitors of HPK1, we generated HPK1 kinase dead (KD) mice which carry a single loss-of-function point mutation in the kinase domain and interrogated the role of kinase activity in immune cells in the context of suppressive factors or the tumor microenvironment (TME). Our data provide novel findings that HKP1 kinase activity is critical in conferring suppressive functions of HPK1 in a wide range of immune cells including CD4+, CD8+, DC, NK to Tregs, and inactivation of kinase domain was sufficient to elicit robust anti-tumor immune responses. These data support the concept that an HPK1 small molecule kinase inhibitor could serve as a novel agent to provide additional benefit in combination with existing immunotherapies, particularly to overcome resistance to current treatment regimens.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Immunity, Cellular*
  • Immunologic Surveillance*
  • Lymphocytes / immunology*
  • Lymphocytes / pathology
  • Mice
  • Mice, Mutant Strains
  • Neoplasms, Experimental / genetics
  • Neoplasms, Experimental / immunology*
  • Point Mutation
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / immunology*
  • Tumor Microenvironment / genetics
  • Tumor Microenvironment / immunology*

Substances

  • hematopoietic progenitor kinase 1
  • Protein Serine-Threonine Kinases

Grants and funding

All authors are employees of Bristol-Myers Squibb (BMS) during the period of this study being conducted. BMS did not play a role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript and only provided financial support in the form of authors’ salaries and research materials. The specific roles of the authors are articulated in the ‘author contributions’ section.