It is very true that lack of sleep causes extra-susceptibility to infectious diseases, to colds and influenza, etc.  But these could all be due to the stress associated with all-nighters, due to overwork, for example, which itself can trigger the initial sleep loss as well.  One biological cause to this phenomenon is an increase in cortisol levels associated with stress, which bears a depressing effect on the immune system.  As mentioned in an earlier section, cortisol levels are independent of sleep or sleep deprivation.

    The immune system involves many complex and intricate mechanisms that cannot all be measured in total, and most immunologists have measured a few limited aspects of cell-mediated immunity (performed mainly by phagocytic T lymphocytes, which also produce phagocytosis-promoting chemicals called lymphokines, such as interferon and interleukin-1 and -2). This category of immunity is usually much easier to measure than humoral immunity (involving B lymphocytes, which produce different antibodies).

    Palmblad and his colleagues (1976) reported that during a period of three stressful nights of sleep deprivation, the rate at which a virus was phagocytosed was depressed.  Also interferon production was measured, and was found to increase during the sleep deprivation as well as on the first day of recovery sleep.  However, these results were not clinically significant, as the researchers themselves pointed out, only statistically so.  Another study performed by Palmblad and other researchers in 1979 did not involve stressed individuals, and is therefore more appropriate to this topic as it rules out the effects of cortisol and catecholamine, products of a stress response which can interfere with overall immune functioning.  The investigators monitored the rates of proliferation of lymphocytes and granulocytes in response to an antigen.  They found that proliferation fell, but remained within normal limits.  Hence, the participants in the study could by no means be considered as ailing from any immune deficiency or failure whatsoever.  If stress is the main factor affecting the immune performance, and not necessarily sleep deprivation, then more stress than was presented in the first study by Palmblad and his colleagues needs to be attained in order to observe some more clinically significant results.  At any rate, we are still in the dark when it comes to assessing the precise effects of lack of sleep on the immune system.  This remains a key area in sleep deprivation studies in need of further research.