Di Renzo M, Pasqui A L, Rubegni P, D'Ascenzo G, De Aloe G, Auteri A, Fimiani M
Department of Clinical Medicine and Immunological Sciences, Azienda Ospedaliera Universitaria Senese, U.O. di Medicina III, Policlinico Le Scotte, 53100 Siena, Italy.
Int J Immunopathol Pharmacol. 2006 Apr-Jun;19(2):391-7. doi: 10.1177/039463200601900215.
Mycobacterium avium complex is a facultative intracellular pathogen that can cause pulmonary disease in immunocompromised individuals. Dendritic cells (DCs) play a central role in protective immunity against mycobacteria. Mycobacterium avium complex infects DCs but does not impair in vitro infected monocytes differentiation into DCs. A 54-year old woman affected by chronic graft-versus-host-disease (cGVHD) was referred to our Division of Dermatology. Immature DCs were generated from her monocytes. One week later she was hospitalized due to a lung infection with Mycobacterium avium complex. Monocyte-derived DCs during Mycobacterium avium infection expressed low levels of CD1a and CD80 as determined by flow cytometry. They also expressed high levels of CD83 and CD86, and when stimulated with LPS for 24 hrs they slightly up-regulated CD83 and did not produce IL12. When monocyte-derived DCs were obtained from the patient after having recovered from the Mycobacterium avium complex infection, they expressed normal levels of CD1a and CD80 and were negative both for CD83 and for CD86. IL12 production in response to LPS was restored. Inhibition of DC maturation by the in vivo infection with Mycobacterium avium may be an immune-evasion mechanism used by the pathogen because incompletely matured DCs may not activate effector T cells efficiently in vivo.
鸟分枝杆菌复合体是一种兼性细胞内病原体,可在免疫功能低下的个体中引起肺部疾病。树突状细胞(DCs)在抗分枝杆菌的保护性免疫中起核心作用。鸟分枝杆菌复合体感染DCs,但不损害体外感染的单核细胞分化为DCs。一名患有慢性移植物抗宿主病(cGVHD)的54岁女性被转诊至我们的皮肤科。从她的单核细胞中产生未成熟的DCs。一周后,她因鸟分枝杆菌复合体肺部感染住院。通过流式细胞术测定,在鸟分枝杆菌感染期间单核细胞衍生的DCs表达低水平的CD1a和CD80。它们还表达高水平的CD83和CD86,并且在用LPS刺激24小时后,它们略微上调CD83且不产生IL12。当从该患者从鸟分枝杆菌复合体感染中恢复后获得单核细胞衍生的DCs时,它们表达正常水平的CD1a和CD80,并且CD83和CD86均为阴性。对LPS的IL12产生得以恢复。鸟分枝杆菌的体内感染对DC成熟的抑制可能是该病原体使用的一种免疫逃避机制,因为未完全成熟的DCs可能在体内不能有效地激活效应T细胞。