Merkel cell polyomavirus and Langerhans cell neoplasm

Autor: Tadashi Yoshino, Jean Gogusev, Yumiko Hashida, Francis Jaubert, Keiko Nagata, Makoto Toi, Noriko Wada, Yasushi Horie, Ichiro Murakami, Masanori Daibata, Michiko Matsushita, Akira Morimoto, Tomonori Higuchi, Takashi Oka, Shinsaku Imashuku, Mitsuko Iguchi, Toshihiko Imamura, Takeshi Iwasaki, Satoshi Kuwamoto, Kazuhiko Hayashi, Junko Nakashima
Jazyk: angličtina
Rok vydání: 2018
Předmět:
Zdroj: Cell Communication and Signaling, Vol 16, Iss 1, Pp 1-12 (2018)
Cell Communication and Signaling : CCS
DOI: 10.1186/s12964-018-0261-y
Popis: Background 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. Methods 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. Results 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. Conclusion 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.
Databáze: OpenAIRE
Externí odkaz:
Nepřihlášeným uživatelům se plný text nezobrazuje