Innate Immunity to Leishmania Infection: Within Phagocytes

Figure 2

(a) Interactions among phagocytes in L. major infection. Upon L. major infection, tissue resident macrophages produce inflammatory cytokines and chemokines [4, 18] that recruit neutrophils and monocytes, which act as effector cells [31, 42] or give rise to inflammatory macrophages and DCs [30, 32]. (b) Neutrophils may either help or prevent parasite clearance by macrophages from B6 and BALB/c mice, respectively [3, 5]. (c) In addition, infected neutrophils help to propagate infection to macrophages, monocytes, and DCs [14, 41]. Moreover, macrophages primed by apoptotic neutrophils became permissive to subsequent infection and induce Th2 responses [21]. (d) DCs infected through efferocytosis of neutrophils fail to activate T lymphocytes [41]. Otherwise, infected DCs go to lymph nodes and induce Th1 responses [29, 32]. (e) Th1 cytokines activate M1 macrophages to kill parasites, whereas Th2 responses induce parasite-permissive M2 macrophages [6, 7].