English: Schematic representation of an immune response to a bacterial infection. Tethering: P-selectins bind to PSGL-1 and tether PMN. Rolling: P-selectins bring PMN near E-selectins and slow rolling commences. Chemokine signalling: slow rolling allows IL-8 binding to CXCR1, then integrin activation results in more adhesive interactions with endothelial ligands. Adhesion: activated LFA-1 binds ICAM-1 or ICAM -2 for firm adhesion. Diapedesis: PMN begins diapedesis by exchanging tight junction molecules with endothelial cells. Migration: PMN follows a gradient of inflammatory chemokines to pathogens. Attack: complement attacks the incoming pathogens, mast cells, and macrophage phagocytose pathogens; toll-like receptor molecules trigger inflammation; antigen presenting dendritic cells express MHC molecules to activate T lymphocytes and to recruit neutrophils. PMN = polymorphonuclear neutrophil; CXCR/CCR = chemokine receptor; s-Le-x = sialyl-Lewis X; LFA = lymphocyte function-associated antigen; PSGL = P-selectin glycoprotein ligand; IL = interleukin; CD = cluster of differentiation; CD11a/CD18 = integrins; RBC = red blood cell; JAM = junctional adhesion molecule; PECAM = platelet endothelial cell adhesion molecule; DC = dendritic cell; MHC = major histocompatibility complex; T cell = T lymphocyte; IP-10 = interferon-gamma induced protein-10; MIP = macrophage inflammatory protein; RANTES = regulated on activation, normal T cell expressed and secreted (CCL5 chemokine); TNF α = tumor necrosis factor alpha; C3a and C5a = complement components 3a and 5a; LTB4 = leukotriene B4.