Project Details
Description
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.
Status | Finished |
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Effective start/end date | 9/1/14 → 8/31/18 |
Funding
- United States-Israel Binational Science Foundation (2013247)
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