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Dimensions of humoral recognition factor depletion in carcinomatous patients.

Summary Humoral recognition factor activity of carcinomatous patients was evaluated by determination of the ability of their serum to support the phagocytosis of a variety of colloidal materials by either Kupffer cells of rat liver slices, isolated rat peritoneal macrophages, or human alveolar macrophages. Kupffer cells and peritoneal and alveolar macrophages phagocytized significantly less colloidal material when incubated in plasma derived from carcinomatous patients than when incubated in plasma obtained from normal control subjects. The inability of serum obtained from cancer patients to support the phagocytosis of diverse colloids was not related to the presence of a phagocytosis-inhibiting factor. The loss in humoral recognition factor activity in neoplasia, therefore, relates to either depletion of HRF or loss of essential cofactors or activators. Since humoral recognition factor contributes to the discriminative ability of the macrophage, the loss of an effective recognition mechanism may contribute to the impairment of immunological rejection mechanisms and to tumor growth and development.