2016
DOI: 10.7150/thno.16180
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Blocking the 4-1BB Pathway Ameliorates Crystalline Silica-induced Lung Inflammation and Fibrosis in Mice

Abstract: Long term pulmonary exposure to crystalline silica leads to silicosis that manifests progressive interstitial fibrosis, eventually leading to respiratory failure and death. Despite efforts to eliminate silicosis, clinical cases continue to occur in both developing and developed countries. The exact mechanisms of crystalline silica-induced pulmonary fibrosis remain elusive. Herein, we find that 4-1BB is induced in response to crystalline silica injury in lungs and that it is highly expressed during development … Show more

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Cited by 43 publications
(41 citation statements)
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“…Silicosis is caused by the inhalation of respirable crystalline silica (CS), which causes persistent inflammation and irreversible fibrosis. Silicosis is a progressive condition that is almost always fatal even when exposure to CS dust has ceased [1][2][3]. It is generally accepted that alveolar macrophages (AMs) are the first and main target cells to contact with CS particles [4].…”
Section: Introductionmentioning
confidence: 99%
“…Silicosis is caused by the inhalation of respirable crystalline silica (CS), which causes persistent inflammation and irreversible fibrosis. Silicosis is a progressive condition that is almost always fatal even when exposure to CS dust has ceased [1][2][3]. It is generally accepted that alveolar macrophages (AMs) are the first and main target cells to contact with CS particles [4].…”
Section: Introductionmentioning
confidence: 99%
“…An agonist-4-1BB mAb seems to aggravate the development of inflammatory metabolic diseases and infectious diseases ( 13 , 16 ). As our previous study demonstrated, blockade of 4-1BB signaling may decrease CS-induced inflammation and pulmonary fibrosis in vivo ( 17 ). Nevertheless, the role (including any regulatory mechanisms) and the profile of expression of 4-1BB in CS-induced pulmonary fibrosis are still unknown.…”
Section: Introductionmentioning
confidence: 64%
“…Back to Th17, Li et al studied alteration of expression in 4-1BB (CD137, TNFRSF9) which is an inducible costimulatory receptor expressed on activated T cells, during lung injury caused by silica using animal model [67]. Then, inhibitor for 4-1BB revealed reduction of Th1 and Th17 responses measured by TNF-α, IFNγ, and I-17A production.…”
Section: Effects Of Silica Particles and Asbestos Fibers On Th17mentioning
confidence: 99%