Chehimi J, Starr S E, Frank I, D'Andrea A, Ma X, MacGregor R R, Sennelier J, Trinchieri G
Division of Allergy, Immunology and Infectious Diseases, Children's Hospital of Philadelphia, Pennsylvania.
J Exp Med. 1994 Apr 1;179(4):1361-6. doi: 10.1084/jem.179.4.1361.
Peripheral blood mononuclear cells (PBMC) from human immunodeficiency virus (HIV)-infected patients, asymptomatic or with acquired immunodeficiency virus, produced 10-fold less interleukin 12 (IL-12) free heavy chain and fivefold less biologically active IL-12 heterodimer than PBMC from uninfected healthy donors when challenged in vitro with the common human pathogen Staphylococcus aureus. In contrast, PBMC from HIV-infected individuals and uninfected control donors produced similar levels of tumor necrosis factor alpha, IL-1 beta, and IL-10, and PBMC from HIV-infected individuals produced three- to fourfold more IL-6 compared with PBMC from uninfected control donors. The defect in IL-12 production is not due to hyperproduction of IL-10, a cytokine exerting an autocrine-negative feedback on IL-12 production, but was directly related to HIV infection, as suggested by the reduced ability of monocytes infected in vitro with HIV to produce IL-12. IL-12 deficiency may be an important component of the immunodeficiency associated with HIV infection.
来自无症状或患有获得性免疫缺陷病毒的人类免疫缺陷病毒（HIV）感染患者的外周血单个核细胞（PBMC），在体外用常见人类病原体金黄色葡萄球菌刺激时，产生的白细胞介素12（IL-12）游离重链比未感染健康供体的PBMC少10倍，生物活性IL-12异二聚体少5倍。相比之下，HIV感染个体和未感染对照供体的PBMC产生的肿瘤坏死因子α、IL-1β和IL-10水平相似，且HIV感染个体的PBMC产生的IL-6比未感染对照供体的PBMC多3至4倍。IL-12产生缺陷并非由于IL-10的过度产生，IL-10是一种对IL-12产生具有自分泌负反馈作用的细胞因子，而是与HIV感染直接相关，体外感染HIV的单核细胞产生IL-12的能力降低表明了这一点。IL-12缺乏可能是与HIV感染相关的免疫缺陷的一个重要组成部分。
