TRIL is involved in cytokine production in the brain following Escherichia coli infection

UMMS Affiliation

Department of Medicine, Division of Infectious Diseases and Immunology

Publication Date


Document Type



Animals; Brain; Carrier Proteins; Cells, Cultured; Chemokine CCL5; Escherichia coli; Escherichia coli Infections; Immunity, Innate; Interleukin-6; Lipopolysaccharides; Membrane Glycoproteins; Membrane Proteins; Mice; Mice, Inbred C57BL; Mice, Knockout; Neuroglia; Poly I-C; Signal Transduction; Toll-Like Receptor 2; Toll-Like Receptor 3; Toll-Like Receptor 4; Toll-Like Receptor 7; Toll-Like Receptor 8; Tumor Necrosis Factor-alpha


Bacterial Infections and Mycoses | Cellular and Molecular Physiology | Immunity | Molecular and Cellular Neuroscience


TLR4 interactor with leucine-rich repeats (TRIL) is a brain-enriched accessory protein that is important in TLR3 and TLR4 signaling. In this study, we generated Tril(-/-) mice and examined TLR responses in vitro and in vivo. We found a role for TRIL in both TLR4 and TLR3 signaling in mixed glial cells, consistent with the high level of expression of TRIL in these cells. We also found that TRIL is a modulator of the innate immune response to LPS challenge and Escherichia coli infection in vivo. Tril(-/-) mice produce lower levels of multiple proinflammatory cytokines and chemokines specifically within the brain after E. coli and LPS challenge. Collectively, these data uncover TRIL as a mediator of innate immune responses within the brain, where it enhances neuronal cytokine responses to infection.

DOI of Published Version



J Immunol. 2014 Aug 15;193(4):1911-9. doi: 10.4049/jimmunol.1302392. Epub 2014 Jul 11. Link to article on publisher's site

Journal/Book/Conference Title

Journal of immunology (Baltimore, Md. : 1950)

Related Resources

Link to Article in PubMed

PubMed ID