Complement-dependent modulation of antitumor immunity following radiation therapy

Michelle Elvington, Melissa Scheiber, Xiaofeng Yang, Katherine Lyons, Dustin Jacqmin, Casey Wadsworth, David Marshall, Kenneth Vanek, Stephen Tomlinson

Research output: Contribution to journalArticlepeer-review

35 Scopus citations


Complement is traditionally thought of as a proinflammatory effector mechanism of antitumor immunity. However, complement is also important for effective clearance of apoptotic cells, which can be an anti-inflammatory and tolerogenic process. We show that localized fractionated radiation therapy (RT) of subcutaneous murine lymphoma results in tumor cell apoptosis and local complement activation. Cotreatment of mice with tumor-targeted complement inhibition markedly improved therapeutic outcome of RT, an effect linked to early increases in apoptotic cell numbers and increased inflammation. Improved outcome was dependent on an early neutrophil influx and was characterized by increased numbers of mature dendritic cells and the subsequent modulation of T cell immunity. Appropriatecomplement inhibition may be a promising strategy to enhance a mainstay of treatment for cancer.

Original languageEnglish
Pages (from-to)818-830
Number of pages13
JournalCell Reports
Issue number3
StatePublished - Aug 7 2014


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