Beck James M
Division of Pulmonary and Critical Care Medicine (111G), University of Michigan Medical School, and Medical Service, Department of Veterans Affairs Medical Center, 2215 Fuller Road, Ann Arbor, MI 48105, USA.
Proc Am Thorac Soc. 2005;2(5):423-7. doi: 10.1513/pats.200507-077JS.
The variety of pulmonary infections encountered in HIV-infected individuals indicates that many components of the host defense network are impaired. In addition to depletion of CD4+ T cell numbers, HIV infection results in functional deficits in CD4+ T cells, CD8+ T cells, and natural killer cells. Although some components of macrophage defense are preserved, lack of activation signals from CD4+ T cells contributes to impaired defense by macrophages. There are few data examining the functional capabilities of neutrophils in the lung, but evidence from peripheral blood neutrophils indicates that defense by these cells is also impaired. An improved understanding of these events in the lung during HIV infection could lead to specific interventions aimed at restoration of deficient function.
在感染HIV的个体中所遇到的肺部感染的多样性表明,宿主防御网络的许多组成部分都受到了损害。除了CD4+ T细胞数量减少外,HIV感染还导致CD4+ T细胞、CD8+ T细胞和自然杀伤细胞出现功能缺陷。尽管巨噬细胞防御的一些组成部分得以保留,但缺乏来自CD4+ T细胞的激活信号导致巨噬细胞的防御功能受损。关于肺部中性粒细胞功能能力的研究数据很少,但来自外周血中性粒细胞的证据表明,这些细胞的防御功能也受到了损害。更好地了解HIV感染期间肺部的这些情况可能会带来旨在恢复功能缺陷的具体干预措施。