The Immune Response to Mycobacterium tuberculosis in HIV-1-Coinfected Persons.

IF 26.9 1区 医学 Q1 IMMUNOLOGY
Hanif Esmail, Catherine Riou, Elsa du Bruyn, Rachel Pei-Jen Lai, Yolande X R Harley, Graeme Meintjes, Katalin A Wilkinson, Robert J Wilkinson
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引用次数: 87

Abstract

Globally, about 36.7 million people were living with HIV infection at the end of 2015. The most frequent infection co-occurring with HIV-1 is Mycobacterium tuberculosis-374,000 deaths per annum are attributable to HIV-tuberculosis, 75% of those occurring in Africa. HIV-1 infection increases the risk of tuberculosis by a factor of up to 26 and alters its clinical presentation, complicates diagnosis and treatment, and worsens outcome. Although HIV-1-induced depletion of CD4+ T cells underlies all these effects, more widespread immune deficits also contribute to susceptibility and pathogenesis. These defects present a challenge to understand and ameliorate, but also an opportunity to learn and optimize mechanisms that normally protect people against tuberculosis. The most effective means to prevent and ameliorate tuberculosis in HIV-1-infected people is antiretroviral therapy, but this may be complicated by pathological immune deterioration that in turn requires more effective host-directed anti-inflammatory therapies to be derived.

hiv -1合并感染者对结核分枝杆菌的免疫应答
截至2015年底,全球约有3670万人感染艾滋病毒。与艾滋病毒-1同时发生的最常见感染是结核分枝杆菌——每年有374,000例死亡可归因于艾滋病毒-结核病,其中75%发生在非洲。艾滋病毒-1感染使结核病的风险增加多达26倍,并改变其临床表现,使诊断和治疗复杂化,并使结果恶化。尽管hiv -1诱导的CD4+ T细胞耗竭是所有这些影响的基础,但更广泛的免疫缺陷也有助于易感性和发病机制。这些缺陷对理解和改进提出了挑战,但也为学习和优化通常保护人们免受结核病侵害的机制提供了机会。预防和改善hiv -1感染者结核病的最有效手段是抗逆转录病毒治疗,但这可能会因病理性免疫恶化而复杂化,这反过来需要衍生出更有效的宿主定向抗炎疗法。
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来源期刊
Annual review of immunology
Annual review of immunology 医学-免疫学
CiteScore
57.20
自引率
0.70%
发文量
29
期刊介绍: The Annual Review of Immunology, in publication since 1983, focuses on basic immune mechanisms and molecular basis of immune diseases in humans. Topics include innate and adaptive immunity; immune cell development and differentiation; immune control of pathogens (viruses, bacteria, parasites) and cancer; and human immunodeficiency and autoimmune diseases. The current volume of this journal has been converted from gated to open access through Annual Reviews' Subscribe to Open program, with all articles published under a CC BY license.
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