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Impaired Responsiveness of Lymphocytes and Serum-inhibitory Factors in Patients with Cancer¹

Department of Surgery, College of Physicians and Surgeons, Columbia University, New York 10032 [N. S.-F., J. B., T. T., K. R.], and French and Polyclinic Medical School, New York, New York 10001 [J. M.]

Cellular immune responsiveness, as measured by lymphocyte transformation in one-way mixed-leukocyte cultures and in phytohemagglutinin (PHA)-stimulated cultures, was evaluated in 60 patients with cancer and in 81 normal controls. The effect produced by sera from these subjects on in vitro transformation of lymphocytes was tested on autologous cells and on homologous responding cells from a constant panel of 10 healthy volunteers.

The responsiveness of lymphocytes from cancer patients to PHA and to a battery of mitomycin-treated allogeneic cells was significantly lower than that of normal controls. Lymphocyte reactivity in the presence of autologous cancer serum was inversely related to the extent of the disease. Pooled normal serum enhanced the responsiveness of lymphocytes from cancer patients but had no such effect on control cultures from healthy subjects. Sera from cancer patients reduced the PHA and mixed-leukocytc culture responsiveness of normal panel lymphocytes to a level that was significantly lower than that found in the presence of sera from healthy controls. The degree of inhibition produced by cancer sera on the blastogenic response of normal lymphocytes increased with advanced disease. Suppression of lymphocyte transformation was markedly greater in mixed-leukocyte cultures than in cultures exposed to PHA.

Out of 60 cancer sera investigated, 23 possessed HL-A reactivity against a random panel of lymphocytes. Our findings demonstrate that serum-inhibitory factors are at least partially responsible for impairment of T-cell responsiveness in cancer patients. It is suggested that isoantigenic modifications on the surface of cancer cells cause the appearance of blocking antibody, with broad cross-reactivity that might bind to the surface of responding and/or target cells.

¹ This work was supported by Grant C-48408 from the State of New York, Department of Health, Kidney Disease Institute.

Received 2/13/73. Accepted 6/25/73.

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