TRIL Is Involved in Cytokine Production in the Brain following Escherichia coli Infection The Journal of Immunology July 11, 2014 Paulina Wochal* , Vijay Rathinam †, Aisling Dunne*,Thaddeus Carlson‡, Wen Kuang§, Katherine J. Seidl‡, J. Perry Hall‡, Lih-Ling Lin‡, Mary Collins‡, Stefan Schattgen†, Christopher R. MacKay†, Caio T. Fagundes*, Susan Carpenter*,†,1,Katherine A. Fitzgerald†,1 and Luke A. J. O’Neill*,1 Author Affiliations *School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland; †Division of Infectious Disease and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605; ‡Inflammation and Immunology Research Unit, Pfizer, Cambridge, MA 02140; and §Global Biotherapeutic Technologies, Pfizer, Andover, MA 01810 Abstract 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.
Posted on: Sat, 12 Jul 2014 13:13:24 +0000
Trending Topics
Recently Viewed Topics
© 2015