Abstract
Autologous plasma, when exposed to complement-activating agents that generate leukotactic activity, induces transient neutropenia after infusion into rabbits. Trypsinized human C5 as well as the chemotactic fragment isolated from zymosan-activated human serum also induces transient neutropenia in rabbits, as do chemotactically active synthetic tripeptides. In each instance the neutropenia-inducing activity parallels the chemotactic activity. Thus, neutropenia-inducing activity and chemotactic activity seem to be related physiologic responses of neutrophils. In vivo margination and/or agglutination of leukocytes may underlie this phenomenon of neutropenia.
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
