Association between peripheral T-Lymphocyte activation and impaired bone mineral density in HIV-infected patients.

Association between peripheral T-Lymphocyte activation and impaired bone mineral density in HIV-infected patients.
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DOI:
10.1186/1479-5876-11-51
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发表时间:
2013-02-28
影响因子:
7.4
通讯作者:
Marchetti G
Marchetti G
中科院分区:
医学2区
文献类型:
--
作者:
Gazzola L;Bellistri GM;Tincati C;Ierardi V;Savoldi A;Del Sole A;Tagliabue L;d'Arminio Monforte A;Marchetti G

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HIV感染患者显示骨质减少/骨质疏松症的早期发病率增加。我们研究了HIV感染者骨代谢紊乱是否与免疫过度激活和免疫过早衰老有关。采用双能X线骨密度仪(DXA)测量骨密度(BMD):低BMD(LBMD)定义为T评分或z评分<-1。检测CD 4 +/CD 8+表型(CD 38/HLA-DR、CD 127、CD 28/CD 57)及外周血IL-7、TNF-α、RANKL、OPG。通过多变量logistic回归评估p <0.05的变量。78例患者入组:55例为LBMD。LBMD患者显示活化HDLADR + CD 4+和CD 8+增加(分别为p = 0.03和p = 0.002)。有趣的是,在组之间没有观察到衰老的⑶ 28-⑶ 57 + ⑶ 4 +/⑶ 8 + T细胞的差异。然而,LBMD患者表现出CD 4 + CD 28-表型降低(p = .04),而CD 28+池(p = .03)较低,这可能反映了高分化CD 28-阴性细胞的凋亡增加。活化的HLADR + CD 4 +/CD 8+和CD 28 + CD 4+细胞与BMD受损独立相关(HLADR + CD 4+百分比每增加一个,AOR = 1.08; CI 95%,1.01 -1.15; p = 0.02; HLADR + CD 8+百分比每增加一个,AOR = 1.07; CI 95%,1.01 -1.11; p = 0.01;每增加一个CD 28 + CD 4+百分比,AOR = 1.06; CI 95%,1.0 -1.13; p = 0.05)。HIV感染患者T细胞活化增强可独立预测BMD紊乱,提示免疫活化在骨质减少/骨质疏松症发病机制中起关键作用,即使在HAART完全抑制病毒的患者中也是如此。本文的在线版本(doi:10.1186/1479-5876-11-51)包含补充材料,可供授权用户使用。
HIV-infected patients display an increased and early incidence of osteopenia/osteoporosis. We investigated whether bone metabolism disorders in HIV-infected patients are related to immune hyperactivation and premature immune senescence. Bone mineral density (BMD) was measured by dual-energy X-ray absorptiometry (DXA): low BMD (LBMD) was defined as T-score or z-score < -1. CD4+/CD8+ phenotype (CD38/HLA-DR, CD127, CD28/CD57), and circulating IL-7, TNF-α, RANKL, OPG were measured. The variables with p < .05 were evaluated by multivariate logistic regression. 78 patients were enrolled: 55 were LBMD. LBMD patients showed increased activated HDLADR + CD4+ and CD8+ (p = .03 and p = .002, respectively). Interestingly, no differences in senescent CD28-CD57 + CD4+/CD8+ T-cells were observed between groups. However, LBMD patients displayed a decreased CD4 + CD28- phenotype (p = .04) at the advantage of the CD28+ pool (p = .03), possibly reflecting heightened apoptosis of highly differentiated CD28-negative cells. Activated HLADR + CD4+/CD8+ and CD28 + CD4+ cells were independently associated with impaired BMD (AOR = 1.08 for each additional HLADR + CD4+ percentage higher; CI 95%,1.01-1.15; p = .02; AOR = 1.07 for each additional HLADR + CD8+ percentage higher; CI 95%,1.01-1.11; p = .01; AOR = 1.06 for each additional CD28 + CD4+ percentage higher; CI 95%,1.0-1.13; p = .05). Heightened T-cell activation in HIV-infected patients independently predicts BMD disorders, suggesting a critical role of immune activation in the pathogenesis of osteopenia/osteoporosis, even in patients achieving full viral suppression with HAART. The online version of this article (doi:10.1186/1479-5876-11-51) contains supplementary material, which is available to authorized users.
DOI: 10.1111/j.1365-2249.2006.03022.x
发表时间: 2006-03-01
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