Depressed PMNC blastogenic response in patients with cancer of the head and neck: a study of IL-2 production, IL-2 consumption, and IL-2 receptor expression

• Published in: The Laryngoscope Vol. 99; no. 2; p. 151
• Main Authors: Eskinazi, D P, Perna, J J, Ershow, A G, Mihail, R C
• Format: Journal Article
• Language: English
• Published: United States 01.02.1989
• Subjects: Adult; Aged; Concanavalin A - pharmacology; Female; Flow Cytometry; Head and Neck Neoplasms - immunology; Head and Neck Neoplasms - metabolism; Humans; Interleukin-2 - metabolism; Leukocytes, Mononuclear - immunology; Leukocytes, Mononuclear - metabolism; Lymphocyte Activation - drug effects; Male; Middle Aged; Phytohemagglutinins - pharmacology; Receptors, Interleukin-2 - analysis; Suppressor Factors, Immunologic - metabolism
• ISSN: 0023-852X
• DOI: 10.1288/00005537-198902000-00006

Approximately two thirds of patients with head and neck cancer have been shown to have peripheral mononuclear cells that exhibit a lowered blastogenic response to the T-cell mitogens, concanavalin A and phytohemagglutinin. To investigate the possible mechanisms of this phenomenon, we measured the amount of activated T-cell lymphokine interleukin-2 present in the supernatant of concanavalin A- or phytohemagglutinin-stimulated peripheral mononuclear cells taken from patients with squamous cell carcinoma of the upper aerodigestive tract. Concentrations were found that were similar to those of healthy subjects. The rate of interleukin-2 consumption and the degree of interleukin-2 receptor expression also were similar for patients and controls. In the course of these experiments, it was noted that differences in blastogenic response between patients and controls were abolished when, 24 hours after the beginning of either concanavalin A or phytohemagglutinin stimulation, the culture supernatant was removed and replaced by fresh medium, containing recombinant interleukin-2 to further sustain cell growth. This suggests that the lower blastogenic response found in patients with head and neck cancer is not due to global immune unresponsiveness, but instead, is caused by selective cell dysfunction(s), which may include the production of a suppressor factor following concanavalin A or phytohemagglutinin stimulation.