Bronke Corine, Palmer Nanette M, Jansen Christine A, Westerlaken Geertje H A, Polstra Abeltje M, Reiss Peter, Bakker Margreet, Miedema Frank, Tesselaar Kiki, van Baarle Debbie
Department of Clinical Viro-Immunology, Sanquin Research and Landsteiner Laboratory, Amsterdam, The Netherlands.
J Infect Dis. 2005 Mar 15;191(6):873-80. doi: 10.1086/427828. Epub 2005 Jan 31.
Since cytomegalovirus (CMV) infection can cause serious clinical complications in immunocompromised individuals, we assessed cellular immune requirements for protection against CMV end-organ disease (CMV-EOD) in human immunodeficiency virus type 1 (HIV-1) infection.
Longitudinal samples from HIV-1-infected patients in the Amsterdam cohort were analyzed. Dynamics of CMV-specific CD8(+) and CD4(+) T cell responses were analyzed by 4-color fluorescence analysis using major histocompatibility class I CMV peptide-tetramers and by intracellular staining for perforin, granzyme B, and interferon (IFN)- gamma after stimulation with CMV-specific stimuli. CMV load was measured in parallel.
In individuals progressing to acquired immunodeficiency syndrome with CMV-EOD, CMV-specific IFN- gamma -producing CD4(+) T cells disappeared during the year before onset of CMV-EOD. This disappearance was accompanied by a sharp increase in CMV load before onset of disease. Despite increasing CMV-specific CD8(+) T cell counts, decreasing CMV-specific IFN- gamma -producing CD8(+) T cell counts were found over time. In contrast, the percentage of CMV-specific perforin- and granzyme B-expressing CD8(+) T cells increased.
Our data indicate that insufficient help of CD4(+) T cells may cause loss of IFN- gamma -producing CD8(+) T cells and loss of control of CMV dissemination. Increasing CMV-infected cell counts in the face of high CMV-specific perforin- and granzyme B-expressing CD8(+) T cell counts may explain the immune pathological characteristics of CMV disease.
由于巨细胞病毒(CMV)感染可在免疫功能低下个体中引起严重的临床并发症,我们评估了在人类免疫缺陷病毒1型(HIV-1)感染中预防CMV终末器官疾病(CMV-EOD)所需的细胞免疫。
分析了阿姆斯特丹队列中HIV-1感染患者的纵向样本。通过使用主要组织相容性复合体I类CMV肽四聚体的四色荧光分析以及在CMV特异性刺激后对穿孔素、颗粒酶B和干扰素(IFN)-γ进行细胞内染色,分析CMV特异性CD8(+)和CD4(+) T细胞反应的动态变化。同时测量CMV载量。
在进展为获得性免疫缺陷综合征并伴有CMV-EOD的个体中,产生CMV特异性IFN-γ的CD4(+) T细胞在CMV-EOD发病前一年消失。这种消失伴随着疾病发作前CMV载量的急剧增加。尽管CMV特异性CD8(+) T细胞计数增加,但随着时间的推移,产生CMV特异性IFN-γ的CD8(+) T细胞计数却在减少。相反,表达CMV特异性穿孔素和颗粒酶B的CD8(+) T细胞百分比增加。
我们的数据表明,CD4(+) T细胞的辅助不足可能导致产生IFN-γ的CD8(+) T细胞丧失以及对CMV传播的控制丧失。在表达CMV特异性穿孔素和颗粒酶B的CD8(+) T细胞计数较高的情况下,CMV感染细胞计数增加可能解释了CMV疾病的免疫病理特征。