Triggering of NOD2 Receptor Converts Inflammatory Ly6C into Ly6C Monocytes with Patrolling Properties.

The signals that regulate the fate of circulating monocytes remain unknown. In the present study, we demonstrate that triggering of the NOD2 receptor by muramyl dipeptide (MDP) converts inflammatory Ly6C monocytes into patrolling Ly6C monocytes. Administration of MDP to Nr4a1 mice, which lack Ly6C monocytes, or to Ly6C-depleted mice led to the emergence of blood-patrolling monocytes with a profile similar to that of Ly6C monocytes, including high expression of CX3CR1 and LFA1.

NR4A1-dependent Ly6C monocytes contribute to reducing joint inflammation in arthritic mice through Treg cells.

Monocytes are central to the physiopathology of arthritis, but their roles in progression and resolution of the disease remain to be clarified. Using NR4A1 mice, which lack patrolling lymphocyte antigen 6C (Ly6C ) monocytes, we found that inflammatory Ly6C monocytes contribute to rapid development of arthritis in a serum transfer-induced arthritis (STIA) model. Our experiments suggest that patrolling monocytes do not promote the initiation and progression of arthritis in mice, as severity of symptoms was amplified in NR4A1 mice.