Asparaginase inhibits the lectin pathway of complement activation

M. P. Keizer, C. Aarts, A. M. Kamp, H. N. Caron, M. D. van de Wetering, D. Wouters, T. W. Kuijpers

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)

Abstract

Oncological treatment has been associated with an increased risk of infection, most often related to therapy-induced pancytopenia. However, limited research has been conducted on the effect of oncological therapy on the complement system, being part of the non-cellular innate immune system. This became the rationale for an observational clinical study (C2012) in which we have investigated the prevalence of transient complement defects. Once we had observed such defects, a correlation of the complement defects to specific clinical parameters or to specific therapeutic regimens was investigated. A prominent defect observed in C2012 was the inhibition of the lectin pathway (LP) of complement activation during the treatment of acute lymphoblastic leukemia (ALL), which we could directly associate to the use of asparaginase (ASNase). Ex-vivo experiments confirmed a direct dose-dependent inhibitory effect of ASNase on the LP functionality.

Original languageEnglish
Pages (from-to)189-192
Number of pages4
JournalMolecular Immunology
Volume93
DOIs
Publication statusPublished - Jan 2018
Externally publishedYes

Keywords

  • Asparaginase
  • Complement activation
  • Lectin pathway
  • Oncology
  • Selective inhibiton

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