Evidence has been presented: (1) that macrophages from experimentally produced inflammatory exudates are capable of phagocyting fully encapsulated Type I pneumococci and group A Friedländer's bacilli in the absence of antibody, (2) that the principal mechanisms involved are those of surface phagocytosis, and (3) that the majority of pneumococci ingested by macrophages in antibody-free preparations are ultimately destroyed.
The relationship of these phenomena to the mechanism of recovery in pneumococcal and Friedländer's bacillus infections has been briefly discussed.
This content is only available as a PDF.
Copyright, 1954, by The Rockefeller Institute for Medical Research New York
1954
You do not currently have access to this content.
