Browse by author
Lookup NU author(s): Dr Arthur Pratt,
Professor John IsaacsORCiD
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
Rheumatoid arthritis (RA) is a systemic inflammatory disease with a predilection for symmetrically distributed diarthroidal joints. It is clinically heterogeneous, with particular disease phenotypes defined according to a complex interplay of genes and the environment. In this chapter we first summarize current knowledge of RA genetic susceptibility, a field which has been transformed in recent years by powerful modern genotyping technologies. The importance of a recently described subclassification for the disease based upon the presence or absence of circulating autoantibodies to citrullinated peptides has further informed genetic studies, and we consider the implications for our understanding of RA pathogenesis. We then review the cellular and molecular processes that initiate and perpetuate joint destruction.
Author(s): Pratt AG, Isaacs JD, Mattey DL
Publication type: Review
Publication status: Published
Journal: Best Practice & Research: Clinical Rheumatology
ISSN (electronic): 1532-1770