Veterans Affairs Center of Excellence for Stress and Mental Health, VA San Diego, CA, USA.
Neuropharmacology. 2012 Feb;62(2):663-73. doi: 10.1016/j.neuropharm.2011.02.027. Epub 2011 Mar 22.
The biological underpinnings for participation of the immune system in the pathogenesis of Posttraumatic Stress Disorder (PTSD) include evidence for cross-talk between the stress and immune systems, as well as more recently discovered roles for immune system mediators in core behavioral functions such as adult neurogenesis, as well as in processes that underlay synaptic plasticity, such as learning and memory. This article reviews the expanding body of literature on immune system mediators in the periphery and the central nervous system (CNS) in chronic PTSD along with the evidence for increased peripheral inflammation, and excess morbidity and mortality. CNS inflammation has been implicated in the pathogenesis of depression. This literature is briefly reviewed, along with evidence for a possible role for CNS inflammation in PTSD symptoms, especially in individuals who have PTSD with co-morbid depression. Whether the immune system is involved in risk and resilience, or evolution of PTSD symptoms following a trauma event remains to be determined, although hypotheses have been advanced. This paper reviews the current evidence including the novel hypothesis that cellular immunity is implicated in PTSD risk and resilience. Potential research implications and directions are discussed. This article is part of a Special Issue entitled 'Post-Traumatic Stress Disorder'.
免疫系统参与创伤后应激障碍（PTSD）发病机制的生物学基础包括应激系统和免疫系统之间的相互作用的证据，以及最近发现免疫系统介质在核心行为功能中的作用，如成年神经发生，以及在支持突触可塑性的过程中，如学习和记忆。本文综述了外周和中枢神经系统（CNS）中免疫系统介质在慢性 PTSD 中的不断扩大的文献，以及外周炎症增加、发病率和死亡率过高的证据。CNS 炎症与抑郁症的发病机制有关。本文简要回顾了这方面的文献，并提出了 CNS 炎症在 PTSD 症状中的可能作用的证据，尤其是在患有 PTSD 合并抑郁的个体中。免疫系统是否参与创伤后风险和韧性，或者创伤后应激障碍症状的演变仍有待确定，尽管已经提出了假设。本文综述了目前的证据，包括细胞免疫与 PTSD 风险和韧性有关的新假设。讨论了潜在的研究意义和方向。本文是一个特刊的一部分，题为“创伤后应激障碍”。
