Immune Response of Plasmacytoid Dendritic Cells Stimulated by Human Papillomavirus (HPV) E6 in an In Vitro System.

Med Sci Monit

Institute of Cancer Research and Basic Medical Sciences of Chinese Academy of Sciences, Cancer Hospital of University of Chinese Academy of Sciences, Zhejiang Cancer Hospital, Hangzhou, Zhejiang, China (mainland).

Published: February 2020

AI Article Synopsis

  • The study investigates how plasmacytoid dendritic cells (pDCs) change when exposed to HPV E6 and co-cultured with Caski cervical cancer cells, to understand their role in cancer development.
  • Results show that HPV E6 increases the expression of certain markers (CD40, MyD88, TRAF6) in pDCs, but when co-cultured with Caski cells, these markers are expressed at lower levels.
  • The findings suggest that pDCs may influence cervical cancer development through regulation of CD40, but more research is needed to clarify the underlying mechanisms.

Article Abstract

BACKGROUND This study aimed to analyze the changes in plasmacytoid dendritic cell (pDC) immunophenotypes when co-cultured with Caski cells and stimulated by human papillomavirus (HPV) E6 in vitro, and thus to discuss the immunoregulatory roles of pDCs in the tumorigenesis of cervical cancer. MATERIAL AND METHODS The immunophenotypic expression of pDCs was analyzed under stimulation of HPV E6 and co-culturing with Caski cells in vitro. RESULTS HPV E6 infection caused significantly increased expression of CD40 in HPV16 M and HPV16 H groups MyD88 in HPV16 M,HPV16 H, and HPV18L groups; and TRAF6 in HPV16 M, HPV16 H, and HPV18L groups. pDCs co-cultured with Caski cells showed significantly lower expression of MyD88 and TRAF6 compared with the control. CONCLUSIONS The expression of MyD88 and TRAF6 might vary in different stages of HPV infection. pDCs might regulate CD40 to participate in the tumorigenesis and progression of cervical cancer, but related mechanisms still need further investigation.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7057736PMC
http://dx.doi.org/10.12659/MSM.919770DOI Listing

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