An Essential Role for RIG-I in Toll-like Receptor-Stimulated Phagocytosis

Ling Kong, Lei Sun, Hongxin Zhang, Qin Liu, Ye Liu, Linhua Qin, Guojun Shi, Jun Hao Hu, Ajing Xu, Yue Ping Sun, Dangsheng Li, Yu Fang Shi, Jing Wu Zang, Jiang Zhu, Zhu Chen, Zhu Gang Wang, Bao Xue Ge

Research output: Contribution to journalArticlepeer-review

68 Scopus citations


Retinoic acid-inducible gene-I (RIG-I) plays an important role in antiviral response by recognizing double-stranded RNA. Here we demonstrate an unanticipated role of RIG-I in Toll-like receptor (TLR)-stimulated phagocytosis. Stimulation with lipopolysaccharide (LPS), a ligand of TLR4, induced the expression of RIG-I in macrophages. Depletion of RIG-I by RNAi or gene targeting inhibited the LPS-induced phagocytosis of bacteria. Cellular processes involved in phagocytosis, such as small GTPase Cdc42/Rac1 activation, actin polymerization, and actin-regulator Arp2/3 recruitment, were also impaired in RIG-I-deficient macrophages activated by LPS. Moreover, RIG-I-/- mice were found to be more susceptible to infection with Escherichia coli as compared to wild-type mice. Thus, the regulatory functions of RIG-I are strikingly broad, including a role not only in antiviral responses but in antibacterial responses as well.

Original languageEnglish (US)
Pages (from-to)150-161
Number of pages12
JournalCell Host and Microbe
Issue number2
StatePublished - Aug 20 2009

All Science Journal Classification (ASJC) codes

  • Parasitology
  • Microbiology
  • Virology




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