When it comes to destroying pathogens, neutrophils aren't picky. Regardless of the type of pathogen, neutrophils recognise the target and migrate to the infection site to engulf it. On the basis of such a standard response, one might expect that all pathogen-recognition signals culminate in the same phagocytic response. On page , Volkmar Heinrich and colleagues now show that this isn't so. Using a dual-micropipette system, they discover that neutrophils elicit target-specific responses to distinct immune threats. Phagocytosis of a zymosan particle – an insoluble fraction from yeast cell walls that mimics fungal infection – begins with protrusion of a transient cellular pedestal that initially pushes the target away. During this phase, pseudopod growth occurs in a direction normal to that of the cell–target contact zone. Phagocytosis of antibody-coated beads similar in size to zymosan particles, however, is quite different: there is no ‘push-out’ phase and the process instead begins with the formation of pseudopodial lamellae that move tangentially to the bead surface. As a result, the beads are engulfed approximately 2.5 times faster. Actin is a key regulator of these differences, playing a dual role in mediating, on the one hand, protrusive deformation following zymosan recognition and, on the other hand, inhibiting this deformation locally during antibody-mediated phagocytosis.
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