Human immunodeficiency virus infection alters antigen-induced cytokine responses in patients with active mycobacterial diseases.

Human immunodeficiency virus infection alters antigen-induced cytokine responses in patients with active mycobacterial diseases.
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人类免疫缺陷病毒感染改变患有活动性分枝杆菌疾病的患者抗原诱导的细胞因子反应。

DOI:
10.1086/515326
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发表时间:
1998
期刊:
The Journal of infectious diseases
影响因子:
--
通讯作者:
Nahmias,A
Nahmias,A
中科院分区:
--
文献类型:
--
作者:
Sousa,AO;Lee,FK;Freiji,R;Lagrange,PH;Nahmias,A

文献摘要

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对29例活动性鸟分枝杆菌病(MAC)和结核分枝杆菌病(TB)患者外周血细胞进行了分枝杆菌抗原诱导的干扰素(IFN)-γ和白细胞介素(IL)-4产生的检测。在MAC患者中,人类免疫缺陷病毒(HIV)感染与产生IFN-γ的患者减少80%相关,导致主要为2型细胞因子谱。结核病患者的HIV感染与产生IL-4的患者增加37%以及1型向0型转变相关。这些质的变化与CD 4+或CD 8+细胞数量无关。HIV感染者IFN-γ和IL-4水平均降低。IFN-γ的定量减少是分泌细胞减少的结果,而不是单细胞水平的下调。播散性疾病仅限于2/5例2型细胞因子谱的HIV感染MAC患者和4/5例0型HIV感染结核病患者。这些结果表明,与AIDS进展平行,分枝杆菌抗原特异性细胞因子谱从1型转变为0型和2型。
Peripheral blood cells from 29 patients with activeMycobacterium avium(MAC) orMycobacterium tuberculosisdiseases were tested for mycobacterial antigen-induced interferon (IFN)-γ and interleukin (IL)-4 production. Among MAC patients, human immunodeficiency virus (HIV) infection was associated with an 80% decrease in those who produced IFN-γ, resulting in a predominantly type 2 cytokine profile. HIV infection in patients with tuberculosis correlates with a 37% increase in those producing IL-4 and a type 1 to type 0 profile shift. These qualitative changes were independent of CD4+ or CD8+ cell numbers. The amounts of both IFN-γ and IL-4 were decreased in the HIV-infected population. Quantitative reduction of IFN-γ was the result of fewer secreting cells rather than a down-regulation at the single-cell level. Disseminated disease was restricted to 2 of 5 HIV-infected MAC patients with a type 2 cytokine profile and 4 of 5 HIV-infected tuberculosis patients with a type 0 profile. These results demonstrated a shift in mycobacterial antigen-specific cytokine profiles from type 1 to type 0 and to type 2, in parallel with AIDS progression.