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Significance Monocytes perpetuate inflammation during autoimmune diseases through chronic sensing of Toll-like receptor (TLR) signals. However, individual monocytes down-regulate their capacity to produce inflammation after an initial TLR-activating event. We now show that continuous TLR9 responsiveness in vivo corresponds to an accumulation of monocytes in peripherally inflamed tissues. Intriguingly, the production and positioning of monocytes occurs independent of the bone marrow, the canonical location of monocyte production during normal homeostasis. Instead, increases in peripheral monocyte numbers are dictated by the accumulation of functionally enhanced monocyte-producing cells in peripherally inflamed tissues. These novel insights into monocyte production and positioning during systemic inflammation implicate local production of TLR-responsive monocytes as a key mechanism contributing to systemic inflammation during autoimmunity.

TLR9-mediated inflammation drives a Ccr2-independent peripheral monocytosis through enhanced extramedullary monocytopoiesis