Model for inflammation-induced HSC cycling. Under steady-state conditions, many HSCs are quiescent, that is, only infrequently divide and generate progeny (left). During infection, however, quiescent HSCs become activated into the cell cycle (right). The signals that induce these processes can either be delivered directly on stimulation of TLRs on HSC by PAMPs or via indirect pathways involving growth factors that are secondarily released from PAMP-sensing bystander or niche cells. The relative importance of direct versus indirect influence on HSC division still needs to be determined.