Figure 2

Human MC and M ϕ differentiation, and distinct subset functions. Human CD14⁺⁺CD16^- classical MCs leave the bone marrow in a CC-chemokine receptor 2 (CCR2)-dependent manner. In the steady state, classical MCs can differentiate into intermediate MCs, then differentiate into patrolling non-classical MCs in circulation. Classical MCs have a high antimicrobial capability due to their potent capacity of phagocytosis, and secrete ROS and IL-10 upon LPS stimulus, whereas intermediate and non-classical MCs secrete inflammatory cytokines, TNFα and IL-1β upon inflammatory stimulation. During inflammation, classical and intermediate MCs are tethered and invade tissue by interaction of complementary pair CCR2/CCL2(MCP1) or/and CCR5/CCL5(RANTES) in a VLA1/VCAM1 dependent manner. MCs then mature to M1Mϕ in tissue and present self-antigen via MHC-I/II to TCR leading to TC activation. Non-classical MCs patrol the vessel wall and invade by interaction of complementary pair of CX3CR1/CCL3 via LAF/ICAM1-dependent manner. TC, T cell; MC, monocyte; Mϕ, macrophage; EC, endothelial cells; inf., inflammatory; α-inf. Anti-inflammatory; TCR, T cell receptor; HLA-DR, human leukocyte antigen DR (a major histocompatibility complex class II (MHC-II)).