Ontology highlight
ABSTRACT: Objective
The mucosal origin hypothesis in rheumatoid arthritis (RA) posits that inhalant exposures, such as cigarette smoke and crystalline silica (c-silica), trigger immune responses contributing to disease onset. Despite the established risk posed by these exposures, the mechanistic link between inhalants, lung inflammation, and inflammatory arthritis remains poorly understood, partly from the lack of a suitable experimental model. As c-silica accelerates autoimmune phenotypes in lupus models and is a recognized risk factor for several autoimmune diseases, we investigated whether c-silica exposure could induce RA-like inflammatory arthritis in mice.Methods
Two arthritis-prone mouse strains, BXD2/TyJ and HLA-DR4 transgenic (DR4-Tg), were exposed to c-silica or PBS via oro
SUBMITTER: Janssen LMF
PROVIDER: S-EPMC11741359 | biostudies-literature | 2025 Jan
REPOSITORIES: biostudies-literature