Protective Role of the MER Tyrosine Kinase via Efferocytosis in Rheumatoid Arthritis Models.

ABSTRACT:

Objective

Rheumatoid arthritis (RA) is a chronic and progressive joint disease. It appears that anti-inflammatory feedback mechanisms that could restrain joint inflammation and restore homeostasis are insufficient to perform this control. In this study, we investigated the contribution of the MER tyrosine kinase-mediated anti-inflammatory response on arthritis and whether targeting MER could be a valid approach to treat RA.

Methods

KRN serum transfer arthritis (KRN STA) was induced in either Mertk-deficient mice or in mice that adenovirally overexpressed Pros1. Human synovial micromasses were treated with MER-specific antibodies or PROS1. Collagen-induced arthritis (CIA) mice were treated with MER-specific agonistic antibodies or by viral overexpression of P

SUBMITTER: Waterborg CEJ 

PROVIDER: S-EPMC5908888 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature