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.

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