Journal article
Non-essential role for TLR2 and its signaling adaptor Mal/TIRAP in preserving normal lung architecture in mice.
SM Ruwanpura, L McLeod, AR Lilja, G Brooks, LF Dousha, HJ Seow, S Bozinovski, R Vlahos, PJ Hertzog, GP Anderson, BJ Jenkins
Plos One | Published : 2013
Abstract
Myeloid differentiation factor 88 (MyD88) and MyD88-adaptor like (Mal)/Toll-interleukin 1 receptor domain containing adaptor protein (TIRAP) play a critical role in transducing signals downstream of the Toll-like receptor (TLR) family. While genetic ablation of the TLR4/MyD88 signaling axis in mice leads to pulmonary cell death and oxidative stress culminating in emphysema, the involvement of Mal, as well as TLR2 which like TLR4 also signals via MyD88 and Mal, in the pathogenesis of emphysema has not been studied. By employing an in vivo genetic approach, we reveal here that unlike the spontaneous pulmonary emphysema which developed in Tlr4(-/-) mice by 6 months of age, the lungs of Tlr2(-/-..
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Funding Acknowledgements
This study was supported by a research grant from the National Health and Medical Research Council (NHMRC, Australia), as well as the Operational Infrastructure Support Program by the Victorian Government of Australia. S.M. Ruwanpura is supported by NHMRC Australian Biomedical Post-doctoral Fellowship. B.J. Jenkins is supported by a Senior Medical Research Fellowship awarded by the Sylvia and Charles Viertel Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.