Suppressive neutrophils require PIM1 for metabolic fitness and survival during chronic viral infection

Peter J. Volberding, Gang Xin, Moujtaba Y. Kasmani, Achia Khatun, Ashley K. Brown, Christine Nguyen, Jennifer S. Stancill, Eli Martinez, John A. Corbett, Weiguo Cui*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


The immune response to a chronic viral infection is uniquely tailored to balance viral control and immunopathology. The role of myeloid cells in shaping the response to chronic viral infection, however, is poorly understood. We perform single-cell RNA sequencing of myeloid cells during acute and chronic lymphocytic choriomeningitis virus (LCMV) infection to address this question. Our analysis identifies a cluster of suppressive neutrophils that is enriched in chronic infection. Furthermore, suppressive neutrophils highly express the gene encoding Proviral integration site for Moloney murine leukemia virus-1 (PIM1), a kinase known to promote mitochondrial fitness and cell survival. Pharmacological inhibition of PIM1 selectively diminishes suppressive neutrophil-mediated immunosuppression without affecting the function of monocytic myeloid-derived suppressor cells (M-MDSCs). Decreased accumulation of suppressive neutrophils leads to increased CD8 T cell function and viral control. Mechanistically, PIM kinase activity is required for maintaining fused mitochondrial networks in suppressive neutrophils, but not in M-MDSCs, and loss of PIM kinase function causes increased suppressive neutrophil apoptosis.

Original languageEnglish (US)
Article number109160
JournalCell reports
Issue number8
StatePublished - May 25 2021


  • LCMV
  • PIM1
  • T cell function
  • chronic viral infection
  • metabolism
  • mitochondrial dynamics
  • single-cell RNA sequencing
  • suppressive neutrophil

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


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