Postoperative immunosuppression

Postoperative immunosuppression refers to the transient reduction in immune function that occurs after surgical procedures. This phenomenon is characterized by decreased cell-mediated immunity, including reductions in T-cell numbers and function, impaired cytokine production (such as TNF‐α, IL‐2, IFN‐γ), and increased apoptosis of lymphocytes[1][2][3]. The mechanisms underlying this state are multifactorial and include the effects of surgical trauma, anesthesia, neuroendocrine stress responses (e.g., catecholamines and glucocorticoids), release of prostaglandins and other soluble mediators, as well as shifts from Th1 to Th2 cytokine profiles[1][2][3][5]. This immunosuppressive window can last from days to weeks post-surgery and is clinically significant because it increases susceptibility to infections, sepsis, poor wound healing, tumor recurrence or metastasis in cancer patients[5][6][7]. It is not a single molecular entity or receptor but rather a complex physiological state involving multiple pathways and cell types. As such, "postoperative immunosuppression" does not correspond to a canonical molecular target suitable for direct pharmacological intervention but represents an important clinical consideration for perioperative management. In summary: "Postoperative immunosuppression" is not itself a molecule or receptor but describes an altered physiological condition following surgery that involves broad suppression of both innate and adaptive immunity. Therefore it should not be classified as a therapeutic target like receptors or enzymes[1][2][3].

Other names

Postoperative immune suppressionSurgery-induced immunosuppressionPost-surgical immunosuppression