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Cellular and Humoral Factors Involved in the Mechanism of the Micro-Leukocyte Adherence Inhibition Reaction¹

Department of Surgical Oncology, Roswell Park Memorial Institute, Buffalo, New York 14263 [M.H.G, A.J.R., J.H.H., E.D.H.], and Department of Surgery, St. James' Hospital, Leeds 9, England [S.H.L.]

To study the cellular basis for specific antigen-induced leukocyte adherence inhibition, enriched populations of B-cells, T-cells, and monocytes were prepared by a two-stage adherence separation procedure from spleen cells of normal C57BL/6J mice and mice bearing progressively growing MCA-38 tumors. The reactor cell undergoing specific antigen-induced adherence inhibition was identified as a monocyte (esterase positive, did not respond to mitogens, and did not bear Thy 1.2 antigen or surface immunoglobulin). Furthermore, an enriched population of MCA-38-sensitized B-cells could program normal monocytes to undergo specific antigen-induced adherence inhibition. In contrast, enriched populations of MCA-38-sensitized T-cells could not program normal nylon wool-adherent cells to undergo antigen-specific adherence inhibition.

Programming of normal monocytes by MCA-38-sensitized B-cells occurs through a soluble mediator and not by direct cell contact. The soluble mediator appears to be immunoglobulin in nature and induced both adherence inhibition and the inhibition of adherence. Thus, in this murine tumor model, leukocyte adherence inhibition appears to be due to programming of monocytes by a secretory product of specifically sensitized B-cells.

¹ Presented at the International Workshop on Leukocyte Adherence Inhibition, May 15 to 17, 1978, Buffalo, N. Y. This work was supported by USPHS Grant CA 22931 from the Department of Surgical Oncology, Tumor Immunology Group, Roswell Park Memorial Institute, 666 Elm Street, Buffalo, N. Y. 14263.

² To whom requests for reprints should be addressed.