There is conflicting evidence about the effect of critical illness on circulating lymphocyte numbers, with reports of both a decrease in total lymphocytes (or T-cell and B-cell subpopulations) and a lymphocytosis after major surgery. Recently, a decrease in the ratio of helper to suppressor T cells, independent of any HIV effect, has been shown in critically ill patients. The mechanisms underlying these changes are multifactorial, although it is likely that cell sequestration to sites of endothelial activation accounts for most fluctuations in circulating counts. As lymphocytes are actively recirculating cells, passing from blood to inflamed site and back through the lymph, with other lymphocytes entering lymph nodes directly through specialized venule endothelium, changes in circulating lymphocyte counts may be unrelated to innate, ornatural „immunity Adaptive.immunity

Lymphocytes Phagocytes the total lymphocyte number.

Specific dysfunction of T cells has been shown after major surgery, with reduced T-cell proliferative responses to commonly used stimulating agents such as phytohemagglutinin; this can be correlated with the extent of surgery. Suppression is also seen in trauma patients and is mediated by a soluble factor, as normal lymphocytes exposed to serum from patients with severe trauma also exhibit reduced proliferative responses which are not seen when cells are exposed to serum from normal volunteers. This suppressive effect can be detected for up to 2 weeks and can be mimicked in animal studies, where 30 per cent hemorrhage reduces mitogen-induced proliferation of T lymphocytes for several days and is temporarily associated with a reduction in IL-2 production ( M.a.n.nlc.kJ..99.3). Likewise, splenocytes have an impaired response to concanavalin A and are associated with depressed production of IL-2, IL-3, IL-6, and interferon-g. Natural killer cell function is also reduced within hours of a burn injury, with function remaining impaired for days; again, this is mediated by a serum factor.

Evidence of specific dysfunction of B cells has not been so clear. With severe injury, total immunoglobulin levels are little altered and may even rise, although this is often due to a non-specific polyclonal increase that may obscure specific functional changes. Some patients exhibit a reduction in primary responses to antigen, while an impaired secondary response to common antigens has been reported in others. Responses to common bacterial antigens tend to remain intact ( Ma.n.niC.k...1993).

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