Yao Yong-ming
Burns Institute, the First Affiliated Hospital of General Hospital of PLA, Beijing 100037, China.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2007 Mar;19(3):138-41.
The excessive inflammatory response accompanied by a dramatic paralysis of cell-mediated immunity following severe trauma, shock and burns appears to be responsible for the increased susceptibility to subsequent sepsis. The mechanism of immunodepression is quite complicated, and it is clearly related to the primary injury or disease and also the treatment. Many studies have been done to elucidate essential processes involved in host innate antimicrobial action activities, including activation of the immune response and also its down-regulation, as well as the mechanisms of pharmacologic immune suppression. Presently, it is recognized that abnormal activation of the innate immune response often leads to macrophage deactivation, loss of antigen presentation capacity, T-cell anergy, and the rapid apoptotic loss of lymphoid tissues, which all contribute to the development of sepsis. Data are accumulating to suggest that restoration of immune function is necessary for the recovery from sepsis and subsequent multiple organ dysfunction syndrome (MODS). A better understanding of the activated innate immunity and its physiological response will help to develop new therapeutical approaches aiming at modulating the immune response in conditions such as sepsis.
严重创伤、休克和烧伤后伴随细胞介导免疫显著麻痹的过度炎症反应似乎是导致随后脓毒症易感性增加的原因。免疫抑制的机制相当复杂，显然与原发性损伤或疾病以及治疗有关。已经进行了许多研究来阐明宿主固有抗菌作用活动中涉及的基本过程，包括免疫反应的激活及其下调，以及药理免疫抑制的机制。目前，人们认识到固有免疫反应的异常激活通常会导致巨噬细胞失活、抗原呈递能力丧失、T细胞无反应性以及淋巴组织的快速凋亡性丧失，所有这些都有助于脓毒症的发展。越来越多的数据表明，免疫功能的恢复对于从脓毒症和随后的多器官功能障碍综合征（MODS）中恢复是必要的。更好地理解激活的固有免疫及其生理反应将有助于开发旨在调节脓毒症等病症中免疫反应的新治疗方法。
