Nicotine Treatment Improves Toll-Like Receptor 2 and Toll-Like Receptor 9 Responsiveness in Active Pulmonary Sarcoidosis

mRNA expression profile of bronchoalveolar lavage fluid cells from patients with idiopathic pulmonary fibrosis and sarcoidosis

“…Clusters formed by genes with changed mRNA expression in IPF samples were implicated in the processes of cell adhesion and T A B L E 2 The most significantly regulated microarray probes: probes with differences of the highest statistical significance as well as the highest and the lowest induced expression for the comparison of IPF vs sarcoidosis BALf cells migration, metalloproteinase expression and negative regulation of cell proliferation. 16 The changes in the expression of mRNA of ribosome proteins in leucocytes recruited into the lungs seem to be an important pathway in the pathobiology of sarcoidosis. Sarcoidosis is believed to be associated with an antigen-specific immune and inflammatory response to yet unidentified antigens.…”

“…Studies have shown enhanced innate activity and Toll-like receptor (TLR) upregulation in BALf cells, 15 but also diminished cytokine production from circulating cells after TLR stimulation in patients with symptomatic compared with asymptomatic pulmonary sarcoidosis. 16 The changes in the expression of mRNA of ribosome proteins in leucocytes recruited into the lungs seem to be an important pathway in the pathobiology of sarcoidosis.…”

Smoking enhances Toll-like receptor-9 responsiveness and type I interferon production in plasmacytoid dendritic cells in patients with cutaneous lupus erythematosus

“…3 Recent studies have shown that antimalarials inhibit TLR-7 and -9 signaling by accumulating inside endosomes and binding to nucleic acids 4 ; nicotine increases the responsiveness of TLR-9 to nucleic acids. 5 These data suggest that the pDCs of smokers who have CLE may be more responsive to agonists, produce more type I interferon than in nonsmokers, and may be less reactive to TLR-9 blockade by antimalarial drugs. This could explain why smokers with CLE have more severe cutaneous involvement 6,7 and reduced efficacy of antimalarial drugs.…”

Adaptive Immunity in Pulmonary Sarcoidosis and Chronic Beryllium Disease

“…Additionally, the number of monocytes undergoing phagocytosis in the blood of sarcoidosis patients is heightened compared to control subjects (24), and circulating monocytes also display higher TLR2 and TLR4 expression (25). Bronchoalveolar lavage (BAL) cells from sarcoidosis patients produce more TNF-α and IL-6 in response to TLR2 agonists than healthy controls, while PBMCs from sarcoidosis patients had impaired TLR2 responses (26,27). Serum amyloid A (SAA) proteins are a group of acute phase inflammatory response proteins that are significantly elevated in the granulomas of sarcoidosis patients and localize to macrophages and giant cells within the granulomas (28).…”