Figure 1

Murine MC and M ϕ differentiation, and distinct subset functions. Mouse Ly6C⁺ MCs leave the bone marrow in a CC-chemokine receptor 2 (CCR2)-dependent manner. In the steady state, Ly6C⁺ MCs differentiate into Ly6C^- MCs in the circulation. Ly6C^- MCs are recruited into normal tissue by interaction of complementary pair CX3CR1/CCL3 via a LAF/ICAM1-dependent manner and become tissue resident Mϕ/DCs. Ly6C⁺ MCs have a high antimicrobial capability due to their potent capacity for phagocytosis, and secrete ROS, TNFα, and IL-1β, whereas Ly6C^- MCs secrete anti-inflammatory cytokine IL-10 upon in vivo bacteria infection. In vascular inflammation, Ly6C⁺ MCs are tethered and invade tissue by interaction complimentary pair of CCR2/CCL2(MPC-1) via a VLA-1/VCAM1-dependent manner, then mature to inflammatory M1Mϕ. M1Mϕ are distinguished by secretion of pro-inflammatory cytokines, TNFα and IL-6 and contribute to tissue degradation and T cell activation. Ly6C^- MCs are recruited to tissue and differentiate into M2Mϕ, which secrete anti-inflammatory cytokine and contribute to tissue repair. TC, T cell; MC, monocyte; M ϕ, macrophage; EC, endothelial cells; DC, dendritic cell; inf., inflammatory; α-inf. Anti-inflammatory; TCR, T cell receptor; HLA-DR, human leukocyte antigen DR (a major histocompatibility complex class II (MHC-II)).