Baena A, Porcelli S A
Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Tissue Antigens. 2009 Sep;74(3):189-204. doi: 10.1111/j.1399-0039.2009.01301.x. Epub 2009 Jun 25.
Mycobacterium tuberculosis is one of the most successful of human pathogens and has acquired the ability to establish latent or progressive infection and persist even in the presence of a fully functioning immune system. The ability of M. tuberculosis to avoid immune-mediated clearance is likely to reflect a highly evolved and coordinated program of immune evasion strategies, including some that interfere with antigen presentation to prevent or alter the quality of T-cell responses. Here, we review an extensive array of published studies supporting the view that antigen presentation pathways are targeted at many points by pathogenic mycobacteria. These studies show the multiple potential mechanisms by which M. tuberculosis may actively inhibit, subvert or otherwise modulate antigen presentation by major histocompatibility complex class I, class II and CD1 molecules. Unraveling the mechanisms by which M. tuberculosis evades or modulates antigen presentation is of critical importance for the development of more effective new vaccines based on live attenuated mycobacterial strains.
结核分枝杆菌是人类最具致病性的病原体之一,它已具备在免疫系统功能完全正常的情况下建立潜伏或进行性感染并持续存在的能力。结核分枝杆菌逃避免疫介导清除的能力很可能反映了一种高度进化且协调的免疫逃逸策略程序,其中包括一些干扰抗原呈递以预防或改变T细胞反应质量的策略。在此,我们综述了大量已发表的研究,这些研究支持了致病性分枝杆菌在多个环节靶向抗原呈递途径这一观点。这些研究揭示了结核分枝杆菌可能通过多种潜在机制主动抑制、破坏或调控主要组织相容性复合体I类、II类分子以及CD1分子的抗原呈递。阐明结核分枝杆菌逃避或调控抗原呈递的机制对于开发基于减毒活分枝杆菌菌株的更有效新型疫苗至关重要。