From ubiquitous antigens to joint-specific inflammation: could local vascular permeability be the missing link?

The mechanisms underlying organ-specific autoimmune diseases are incompletely understood. In particular, it is still unclear how autoantibodies, often against ubiquitous antigens, can cause pathology preferentially in certain tissues. Recently, Binstadt and colleagues, using observations in the K/BxN murine arthritis model, suggested novel pathways underlying the site-specific localization of inflammation driven by immune complexes. In this commentary, we discuss these findings, the problems related to their general applicability and the implications for future research.