| First Author | Kumar H | Year | 2011 |
| Journal | J Immunol | Volume | 186 |
| Issue | 2 | Pages | 994-1000 |
| PubMed ID | 21148033 | Mgi Jnum | J:168788 |
| Mgi Id | MGI:4938234 | Doi | 10.4049/jimmunol.1002094 |
| Citation | Kumar H, et al. (2011) NLRC5 deficiency does not influence cytokine induction by virus and bacteria infections. J Immunol 186(2):994-1000 |
| abstractText | Nucleotide-binding domain and leucine rich repeat containing gene family receptors (NLRs) are cytosolic proteins that respond to a variety of pathogen and host components to induce inflammatory cytokines. NLRC5 is a recently identified member of the NLR family that has been implicated in positive and negative regulation of antiviral innate immune responses. To clarify whether NLRC5 controls antiviral innate immunity in vivo, we generated NLRC5-deficient mice. Macrophages and dendritic cells derived from NLRC5-deficient mice induced relatively normal levels of IFN-beta, IL-6, and TNF-alpha after treatment with RNA viruses, DNA viruses, and bacteria. The serum cytokine levels after polyinosinic-polycytidylic acid infection were also comparable between control and NLRC5-deficient mice. NLRC5 overexpression promoted IL-1beta production via caspase-1, suggesting that NLRC5 constitutes an inflammasome. However, there was no reduction of IL-1beta in NLRC5-deficient cells in response to known inflammasome activators, suggesting that NLRC5 controls IL-1beta production through an unidentified pathway. These findings indicate that NLRC5 is dispensable for cytokine induction in virus and bacterial infections under physiologic conditions. |
