Toll-like receptors and autophagy in interstitial lung diseases.
Interstitial lung diseases (ILDs) include a number of diseases whose pathogenesis still is not fully understood. Idiopathic pulmonary fibrosis (IPF), the most frequent and severe form of ILDs is an epithelial-driven disease and the treatment consists of the use of antifibrotic agents. In the rest of ILDs an inflammation-driven pathway is believed to be the main pathogenetic mechanism and treatment consists of the use of immunomodulatory agents. In both groups it is believed that infection can play an important role in the development and progression of the diseases. The immune system can recognize exogenous threats or endogenous stress through specialized receptors namely pattern recognition receptors (PRRs) which in turn, initiate downstream signaling pathways to control immune responses. Recently, a link between PRRs and autophagy, a specialized biological process involved in maintaining cellular homeostasis but also involved in various immunologic processes, has been described. In this review, we focus on the reciprocal influences of PRRs with particular emphasis on Toll-like receptors and autophagy in modulating innate immune responses.
Interstitial Lung Disease Unit, Royal Brompton Hospital, SW3 6NP London, UK. Electronic address: G.Margaritopoulos@rbht.nhs.uk.
George A
GA
Margaritopoulos
Laboratory of Cellular and Molecular Pneumonology, Medical School, University of Crete, Heraklion 71110, Greece.
Ismini
I
Lasithiotaki
Laboratory of Cellular and Molecular Pneumonology, Medical School, University of Crete, Heraklion 71110, Greece.
Katerina M
KM
Antoniou
D000818:Animals; D001343:Autophagy; D006801:Humans; D017563:Lung Diseases, Interstitial / Q000378:metabolism* / Q000473:pathology*; D051193:Toll-Like Receptors / Q000378:metabolism*
D051193:Toll-Like Receptors
Autophagy; Idiopathic pulmonary fibrosis; Infection; Inflammation; Innate immunity; Toll-like receptors