Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA 19140, USA.
J Neuroimmune Pharmacol. 2011 Mar;6(1):20-7. doi: 10.1007/s11481-010-9247-2. Epub 2010 Oct 19.
The interactions between the immune and nervous systems are very complex, and yet our understanding of these interactions is still relatively limited. The neuroinflammatory reaction that can accompany HIV infection occurs because of a cascade of events that appears to require the migration of HIV-infected cells across the blood-brain barrier. In susceptible individuals, this leads to inflammatory processes which can include substantial changes in neuronal function. It is possible to consider the inflammatory events to be composed of two essential processes. The first process is cellular traffic, and the second, is the expression and recognition of the various pro-inflammatory and/or toxic mediators. The added complication of drug abuse adds complexity to the traffic and mediator release events, and depending on the specific drug being abused, the disease can be exacerbated in these individuals. An understanding of the fine details of these mediator and traffic processes should provide useful targets for therapeutic intervention to attenuate disease associated with HIV infection.
免疫系统和神经系统之间的相互作用非常复杂,但我们对这些相互作用的理解仍然相对有限。伴随 HIV 感染而发生的神经炎症反应是一系列事件的结果,这些事件似乎需要 HIV 感染细胞穿过血脑屏障迁移。在易感染个体中,这会导致炎症过程,其中可能包括神经元功能的实质性变化。可以认为炎症事件由两个基本过程组成。第一个过程是细胞迁移,第二个过程是各种促炎和/或毒性介质的表达和识别。药物滥用的额外复杂性增加了交通和介质释放事件的复杂性,并且取决于被滥用的特定药物,这些个体的疾病可能会加重。对这些介质和交通过程的细微细节的理解应为治疗干预提供有用的靶点,以减轻与 HIV 感染相关的疾病。