Human cytomegalovirus and autoimmune disease.
Human cytomegalovirus and autoimmune disease.
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DOI：
10.1155/2014/472978
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发表时间：
2014
影响因子：
--
通讯作者：
Hengel H
中科院分区：
文献类型：
--
作者：
Halenius A;Hengel H
人巨细胞病毒（HCMV）是疱疹病毒家族β亚群的原型致病成员。HCMV的一系列特征，如其在多种组织中的裂解性复制、通过潜伏期和间歇性再活化的终身持续性、非常大的蛋白质组以及对适应性和先天免疫的广泛操纵，使得HCMV成为参与自身免疫性疾病的高知名度候选者。我们调查了现有文献中关于HCMV与自身免疫性疾病发作或加重相关的报道。HCMV与系统性红斑狼疮（SLE）、系统性硬化症（SSc）、1型糖尿病和类风湿性关节炎（RA）之间的因果关系已被文献证实。然而，HCMV血清阳性率和疾病之间的明确联系尚不能确定，因此HCMV是否在疾病的发生中起共同作用仍是一个未知数。为了得到令人信服的结论，未来必须进行基于人群的前瞻性研究。已经提出了HCMV可能有助于自身免疫性疾病过程的特定免疫致病机制，例如，SSc中的UL 94和SLE患者中的UL 83/pp 65的分子模拟，以及RA患者中通过诱导和扩增CD 4 +/CD 28 − T细胞而加重关节炎症。需要进一步的研究来验证这些发现，并为有针对性的治疗干预奠定基础。
Human cytomegalovirus (HCMV) represents a prototypic pathogenic member of the β-subgroup of the herpesvirus family. A range of HCMV features like its lytic replication in multiple tissues, the lifelong persistence through periods of latency and intermitting reactivation, the extraordinary large proteome, and extensive manipulation of adaptive and innate immunity make HCMV a high profile candidate for involvement in autoimmune disorders. We surveyed the available literature for reports on HCMV association with onset or exacerbation of autoimmune disease. A causative linkage between HCMV and systemic lupus erythematosus (SLE), systemic sclerosis (SSc), diabetes mellitus type 1, and rheumatoid arthritis (RA) is suggested by the literature. However, a clear association of HCMV seroprevalence and disease could not be established, leaving the question open whether HCMV could play a coresponsible role for onset of disease. For convincing conclusions population-based prospective studies must be performed in the future. Specific immunopathogenic mechanisms by which HCMV could contribute to the course of autoimmune disease have been suggested, for example, molecular mimicry by UL94 in SSc and UL83/pp65 in SLE patients, as well as aggravation of joint inflammation by induction and expansion of CD4+/CD28− T-cells in RA patients. Further studies are needed to validate these findings and to lay the grounds for targeted therapeutic intervention.
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影响因子：
3.7
作者：
Arnolds, Kathleen L.;Lares, Angela P.;Spencer, Juliet V.
通讯作者：
Spencer, Juliet V.
DOI：
10.1196/annals.1422.059
发表时间：
2007-01-01
期刊：
AUTOIMMUNITY, PT D
影响因子：
--
作者：
Barzilai, O.;Sherer, Y.;Shoenfeld, Y.
通讯作者：
Shoenfeld, Y.
影响因子：
158.5
作者：
Arbuckle, MR;McClain, MT;Harley, JB
通讯作者：
Harley, JB
影响因子：
5.6
作者：
Amsler, Lisi;Verweij, Marieke C.;DeFilippis, Victor R.
通讯作者：
DeFilippis, Victor R.
影响因子：
4.4
作者：
Deshpande, S;Zheng, M;Rouse, BT
通讯作者：
Rouse, BT