期刊
PAPILLOMAVIRUS RESEARCH
卷 1, 期 -, 页码 12-21出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.pvr.2015.05.001
关键词
Papillomavirus; HPV16; Langerhans cells; Immune escape
类别
资金
- NIH [RO1 CA074397, RC2 CA148298]
- L.K. Whittier Foundation
- Karl H. and Ruth M. Balz Trust
- SC CTSI (NIH/ NCRR/NCATS) [TL1TR000132]
- ARCS Foundation
- NCI [P30CA014089]
Human papillomaviruses (HPV) establish persistent infections because of evolved immune evasion mechanisms, particularly HPV-mediated suppression of the immune functions of Langerhans cells (LC), the antigen presenting cells of the epithelium. Polyinosinic-polycytidilic acid (Poly-I:C) is broadly immunostimulatory with the ability to enhance APC expression of costimulatory molecules and inflammatory cytokines resulting in T cell activation. Here we investigated the activation of primary human LC derived from peripheral blood monocytes after exposure to HPV16 virus like particles followed by treatment with stabilized Poly-I:C compounds (s-Poly-I:C), and their subsequent induction of HPV16-specific T cells. Our results indicate that HPV16 particles alone were incapable of inducing LC activation as demonstrated by the lack of costimulatory molecules, inflammatory cytokines, chemokine-directed migration, and HPV16-specific CD8** T cells in vitro. Conversely, s-Poly-LC caused significant upregulation of costimulatory molecules and induction of chemokine-directed migration of LC that were pre-exposed to HPV16. In HLA-A*0201-positive donors, s-Poly-I:C treatment was able to induce CD8(+) T cell immune responses against HPV16-derived peptides. Thus, s-Poly -LC compounds are attractive for translation into therapeutics in which they could potentially mediate clearance of persistent HPV infection. (C) 2015 The Authors. Published by Elsevier B.V.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据