Peter James Richards

TL;DR: A critical role is established for the soluble IL-6R in joint inflammation in rheumatoid arthritis using an experimental arthritis model and specific blockade of soluble IL -6R signaling in wild-type mice using soluble gp130 ameliorated disease.

TL;DR: It is shown that in several chronic inflammatory diseases, such as chronic inflammatory bowl disease, peritonitis, and rheumatoid arthritis, as well as in colon cancer, transsignaling via the sIL-6R complexed to IL-6 is a crucial point in the maintenance of the disease.

TL;DR: It is proposed that within the context of arthritis pathology HtrA1 contributes to cartilage degradation through both direct and indirect mechanisms.

TL;DR: This study combines genetic approaches and intervention strategies to describe a fundamental requirement for IL-6-mediated STAT3 signaling in orchestrating the inflammatory infiltrate in monoarticular and systemic models of experimental arthritis, and suggests that selective inhibition ofIL-6 trans signaling may provide a more refined intervention strategy for blocking IL- 6-driven proarthritic activities.

TL;DR: The data suggest that HtrA1 is directly involved in the β-amyloid pathway as it degrades various fragments of amyloid precursor protein while an Htr a1 inhibitor causes accumulation of Aβ in astrocyte cell culture supernatants.