Merkel cell polyomavirus and Langerhans cell neoplasm.
Merkel cell polyomavirus and Langerhans cell neoplasm.
复制标题
DOI：
10.1186/s12964-018-0261-y
复制
发表时间：
2018-08-22
期刊：
影响因子：
--
通讯作者：
Jaubert F
中科院分区：
文献类型：
--
作者：
Murakami I;Wada N;Nakashima J;Iguchi M;Toi M;Hashida Y;Higuchi T;Daibata M;Matsushita M;Iwasaki T;Kuwamoto S;Horie Y;Nagata K;Hayashi K;Oka T;Yoshino T;Imamura T;Morimoto A;Imashuku S;Gogusev J;Jaubert F
花粉、食物、传染性病原体等各种外部因素与人体敏感性之间的关系是存在的，并且根据个人的健康状况而变化。例如，我们认为，默克尔细胞多瘤病毒（MCPyV），皮肤中的常驻病毒，其致病潜力是可变的，并取决于个体的反应程度。通常以亚临床感染形式与人类相关的MCPyV以及Epstein-Barr病毒被认为在不同程度上参与几种肿瘤和炎性疾病。在这篇综述中，我们涵盖了两种类型的朗格汉斯细胞肿瘤，朗格汉斯细胞肉瘤（LCS）和朗格汉斯细胞组织细胞增生症（LCH），代表无论是肿瘤性或炎症性疾病引起的MCPyV。我们对之前的分析进行了荟萃分析，包括MCPyV-DNA的定量PCR、蛋白质组学、构建IL-17内分泌模型和白细胞介素-1（IL-1）激活环模型的免疫组织化学以及其他组的数据。我们已经表明，在这两种不同的肿瘤中，存在与MCPyV作为致病因子相关的亚组。相比之下，LCS，不同于LCH，是一种肿瘤性病变（或肉瘤），不存在炎性肉芽肿，常见于老年人。LCH是一种朗格汉斯样异常细胞的增殖性疾病，其携带参与RAS/MAPK信号通路的基因突变。我们发现MCPyV可能参与了LCH的发生。我们假设LCS的一个亚组根据参与默克尔细胞癌发病机制的相同机制发展。我们认为LCH是由基因突变引起的炎症过程发展而来的。我们假设MCPyV感染触发了LCH发病机制下的IL-1激活环，并提出了一个新的三因素模型。
The relationship between various external agents such as pollen, food, and infectious agents and human sensitivity exists and is variable depending upon individual’s health conditions. For example, we believe that the pathogenetic potential of the Merkel cell polyomavirus (MCPyV), the resident virus in skin, is variable and depends from the degree of individual’s reactivity. MCPyV as well as Epstein-Barr virus, which are normally connected with humans under the form of subclinical infection, are thought to be involved at various degrees in several neoplastic and inflammatory diseases. In this review, we cover two types of Langerhans cell neoplasms, the Langerhans cell sarcoma (LCS) and Langerhans cell histiocytosis (LCH), represented as either neoplastic or inflammatory diseases caused by MCPyV. We meta-analyzed both our previous analyses, composed of quantitative PCR for MCPyV-DNA, proteomics, immunohistochemistry which construct IL-17 endocrine model and interleukin-1 (IL-1) activation loop model, and other groups’ data. We have shown that there were subgroups associated with the MCPyV as a causal agent in these two different neoplasms. Comparatively, LCS, distinct from the LCH, is a neoplastic lesion (or sarcoma) without presence of inflammatory granuloma frequently observed in the elderly. LCH is a proliferative disease of Langerhans-like abnormal cells which carry mutations of genes involved in the RAS/MAPK signaling pathway. We found that MCPyV may be involved in the development of LCH. We hypothesized that a subgroup of LCS developed according the same mechanism involved in Merkel cell carcinoma pathogenesis. We proposed LCH developed from an inflammatory process that was sustained due to gene mutations. We hypothesized that MCPyV infection triggered an IL-1 activation loop that lies beneath the pathogenesis of LCH and propose a new triple-factor model.
登录
查看更多内容
DOI：
10.4049/jimmunol.0902336
发表时间：
2010-04-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Allen CE;Li L;Peters TL;Leung HC;Yu A;Man TK;Gurusiddappa S;Phillips MT;Hicks MJ;Gaikwad A;Merad M;McClain KL
通讯作者：
McClain KL
DOI：
10.1084/jem.20130977
发表时间：
2014-04-07
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Berres ML;Lim KP;Peters T;Price J;Takizawa H;Salmon H;Idoyaga J;Ruzo A;Lupo PJ;Hicks MJ;Shih A;Simko SJ;Abhyankar H;Chakraborty R;Leboeuf M;Beltrão M;Lira SA;Heym KM;Bigley V;Collin M;Manz MG;McClain K;Merad M;Allen CE
通讯作者：
Allen CE
影响因子：
56.9
作者：
Asagiri, Masataka;Hirai, Toshitake;Takayanagi, Hiroshi
通讯作者：
Takayanagi, Hiroshi
影响因子：
20.3
作者：
Badalian-Very, Gayane;Vergilio, Jo-Anne;Rollins, Barrett J.
通讯作者：
Rollins, Barrett J.
影响因子：
2.6
作者：
Chilosi, Marco;Facchetti, Fabio;Doglioni, Claudio
通讯作者：
Doglioni, Claudio