J.Jpn. Surg. Soc.. 104(12): 822-827, 2003

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Feature topic

MECHANISM OF IMMUNE SUPPRESSION AFTER SURGICAL STRESS AND HOST DEFENSE AGAINST INFECTION

Suppression of cellular immunity secondary to decreased immunocyte function is one of the surgical stress-induced biological responses. Monocytes/macrophages, natural killer (NK) cells, lymphocytes, and neutrophils play an important role in this immune system. These immunity charge cells are expressed through various surface antigens, such as major histocompatibility complex (MHC) class antigens, T cell receptors, and the cytokines interferon-gamma, interleukin (IL)-2, and IL-12. MHC class II antigen expression of monocytes and the cytokine production of CD4+T cells are decreased after surgical stress. In this immune-suppressed condition, patients after surgical stress can easily experience infectious complications, and therefore the up-regulation of the immune system is necessary to avoid those complications. Recently, the role of natural immunity as a defense system against infection has received attention. The discovery of Toll-like receptor families revealed how the macrophage system cells recognize microorganisms. Furthermore, liver natural killer (NK) cells and NK T cells are important to induce the Th1 immune response in bacterial peritonitis. In this manuscript, we explain the mechanism of immune suppression after surgical stress and the host defense against infection by analyzing cytokine production and surface membrane molecules in mononuclear cells.

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