ABSTRACT
The neutrophil plays a central role in the pathogenesis of many inflammatory disorders of the vasculature. The presence of neutrophils in vasculitic lesions, including those of Wegener's granulomatosis, leukocytoclastic vasculitis, etc., bears witness to this (Fig. I). Cochrane's classic demonstration that neutrophils are required for tissue injury in Arthus vasculitis, which does not develop in rabbits depleted of neutrophils, lends further support to the hypothesis that neutrophils are not passive bystanders in these lesions (l ,2). In the human, counterparts to the Arthus reaction include immune complex-mediated vasculitides such as cryoglobulinemia, Schonlein-Henoch purpura, and vasculitis associated with hepatitis Band C infections. The neutrophil is also featured prominently in many antibody-associated diseases, for instance, Goodpasture's syndrome, the ANCAassociated vasculitides (e.g., polyarteritis nodosa, Wegener's granulomatosis, microscopic polyarteritis), as well as vasculitides putatively associated with antiendothelial antibodies (e.g., Kawasaki disease). Regardless of the etiology, the neutrophil clearly contributes to vessel injury in many different types of vasculitides.
