We hypothesize that under steady state conditions the resident synovial macrophage population functions to prevent inflammation; however, during inflammatory arthritis the non-classical monocytes extravasate into the joint and become inflammatory macrophages leading to destructive RA-like disease. Following a signal that induces resolution of disease (i.e. anti-TNF therapy), macrophages alter their phenotype and become polarized towards a regulatory/remission in situ without the requirement of monocytes from circulation.
|Effective start/end date||9/1/14 → 8/31/18|
- United States-Israel Binational Science Foundation (2013247)