LEUKOCYTOSIS AND NATURAL-KILLER-CELL FUNCTION PARALLEL NEUROBEHAVIORAL FATIGUE-INDUCED BY 64 HOURS OF SLEEP-DEPRIVATION

The hypothesis that sleep deprivation depresses immune function was te sted in 20 adults, selected on the basis of their normal blood chemist ry, monitored in a laboratory for 7 d, and kept awake for 64 h. At 220 0 h each day measurements were taken of total leukocytes (WBC), monocy tes, granulocytes, lymphocytes, eosinophils, erythrocytes (RBC), B and T lymphocyte subsets, activated T cells, and natural killer (NK) subp opulations (CD56/CD8 dual-positive cells, CD16-positive cells, CD57-po sitive cells). Functional tests included NK cytotoxicity, lymphocyte s timulation with mitogens, and DNA analysis of cell cycle. Sleep loss w as associated with leukocytosis and increased NK cell activity. At the maximum sleep deprivation, increases were observed in counts of WBC, granulocytes, monocytes, NK activity, and the proportion of lymphocyte s in the S phase of the cell cycle. Changes in monocyte counts correla ted with changes in other immune parameters. Counts of CD4, CD16, CD56 , and CD57 lymphocytes declined after one night without sleep, whereas CD56 and CD57 counts increased after two nights. No changes were obse rved in other lymphocyte counts, in proliferative responses to mitogen s, or in plasma levels of cortisol or adrenocorticotropin hormone. The physiologic leukocytosis and NK activity increases during deprivation were eliminated by recovery sleep in a manner parallel to neurobehavi oral function, suggesting that the immune alterations may be associate d with biological pressure for sleep.