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Immunological Mechanisms of Tube Leukocyte Adherence Inhibition¹

Montreal General Hospital Research Institute, Montreal, Quebec, Canada H3G 1A4

Enrichment and depletion of certain peripheral blood leukocyte (PBL) populations from patients indicated that the indicator and/or reactive cell manifesting nonadherence in the presence of appropriate tumor antigen was phagocytic, was glass adherent in the absence of tumor antigen, and had cell surface Fc receptors. The reactive cell, therefore, appeared to be the circulating monocyte. Two different experiments failed to show that T-lymphocytes released mediators that were responsible for inhibiting monocyte glass adherence. Immunoglobulin G purified from the sera of leukocyte adherence inhibition (LAI)-reactive patients was shown to "arm" normal PBL to react to the specific antigen. Patients with a limited tumor burden had free cytophilic immunoglobulin G antitumor antibody in their serum, whereas the serum of patients with large tumor burdens, whose leukocytes did not react in the tube LAI, did not arm. The mechanism whereby the specific tumor antigen appeared to be recognized was through the binding of cytophilic immunoglobin G antitumor antibody to Fc receptors on the cell surface of the monocyte. The serum of the nonreactive patient contained free tumor antigenic determinants capable of absorbing free cytophilic antitumor antibody or when preincubated with reactive leukocytes abrogating their LAI responsiveness. Blocking was immunologically specific; therefore, the specificity resides in the tumor antigenic determinant. The tumor antigen coat was removed by gentle trypsinization of the surface of the monocyte, and this restored the capacity of the monocyte to react in the tube LAI. About 20% of the PBL population were responsible for the manifestation of LAI when incubated with the sensitizing antigen. PBL from patients with metastatic cancer showed an identical mean nonadherence when incubated with the specific and the nonspecific cancer extracts. The mean nonadherence of PBL from patients with metastatic cancer was similar to the mean nonadherence of leukocytes from patients with limited cancer when incubated with the sensitizing antigen. Hence, we propose that the increased nonadherence to glass of leukocytes from patients with metastatic cancer results when the LAI-reactive cells (monocytes) are coated in vivo with tumor-specific antigen. Thus, the nonadherence of leukocytes from patients with limited and metastatic cancer is induced by the binding of tumor-specific antigen to the cell surface of the monocyte; in the former instance, binding occurs in vitro and in the latter in vivo.

¹ Presented at the International Workshop on Leukocyte Adherence Inhibition, May 15 to 17, 1978, Buffalo, N. Y.

² Presenter. To whom reprint requests should be addressed, at Montreal General Hospital, 1650 Cedar Avenue, Montreal, Quebec, Canada H3G 1A4.