Plasmacytoid dendritic cells are present in cervical carcinoma and become activated by human papillomavirus type 16 virus-like particles

Bontkes, Hetty J.; Ruizendaal, Janneke J.; Kramer, Duco; Meijer, Chris J.L.M.; Hooijberg, Erik

doi:10.1016/j.ygyno.2004.10.040

Cited by 43 publications

(31 citation statements)

References 20 publications

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“…pDC link innate and adaptive immunity, and produce type I IFN following activation through TLR-7 and -9 by microbes and microbial products, thus participating in the protection against infections (10,21). However, pDC were also implicated in a variety of sterile inflammatory conditions (10,22,23), and infiltrate a broad range of solid tumors such as head and neck cancer (24), ovarian cancer (25), cervical carcinoma (26), lung cancer (27), thyroid cancer (28), breast cancer (29), and melanoma (30). Despite the increasing number of observations about pDC presence in solid tumors, the nature of the signals they receive within the tumor microenvironment is not known (221).…”

Section: Discussionmentioning

confidence: 99%

Breast Cancer Cell–Derived GM-CSF Licenses Regulatory Th2 Induction by Plasmacytoid Predendritic Cells in Aggressive Disease Subtypes

et al. 2015

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Reciprocal interactions between tumor cells and their microenvironment vitally impact tumor progression. In this study, we show that GM-CSF produced by primary breast tumor cells induced the activation of plasmacytoid predendritic cells (pDC), a cell type critical to anti-viral immunity. pDC that expressed the GM-CSF receptor were increased in breast tumors compared with noninvolved adjacent breast tissue. Tumoractivated pDC acquired na€ ve CD4 þ T-cell stimulatory capacity and promoted a regulatory Th2 response. Finally, the concomitant increase of GM-CSF and pDC was significantly associated with relatively more aggressive breast cancer subtypes. Our results characterize the first tumor-derived factor that can activate pDC to promote a regulatory Th2 response, with implications for therapeutic targeting of a tumor-immune axis of growing recognition in its significance to cancer. CancerRes; 75(14); 2775-87. Ó2015 AACR.

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Section: Discussionmentioning

confidence: 99%

Breast Cancer Cell–Derived GM-CSF Licenses Regulatory Th2 Induction by Plasmacytoid Predendritic Cells in Aggressive Disease Subtypes

et al. 2015

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“…Lenz and colleagues (21) showed in an in vitro study that HPV-16 is bound by freshly isolated immature pDCs and CpG maturated pDCs, that internalization of the virus preferentially occurs in immature pDCs, and that it induces the production of IFN-a and IL-6, important factors for the production of antibodies. Bontkes and colleagues (22) showed that pDCs are present in cervical cancer lesions and that HPV-16 virus-like particles are able to activate pDCs. In the dermal layer of VINafflicted skin, no differences for cell numbers of immature mDCs were observed, but the more mature CD208 + (DC-Lamp) DCs were significantly increased.…”

Section: Interestingly Mulvany and Allen (19) Observed Increased Nummentioning

confidence: 99%

Disturbed Patterns of Immunocompetent Cells in Usual-Type Vulvar Intraepithelial Neoplasia

Seters¹,

Beckmann²,

Heijmans-Antonissen³

et al. 2008

Cancer Research

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Genital infection with human papillomavirus (HPV) is usually transient, as the immune system is capable of eliminating the virus. When immunity ''fails'' and the infection persists, vulvar intraepithelial neoplasia (VIN) may develop. In this study, we examined the distribution of inflammatory cells in 51 patients with HPV-associated usual-type VIN and in 19 healthy controls. Frozen vulvar tissue samples were tested for the presence of HPV-DNA, and immunohistochemical staining for the markers CD1a, CD207, CD208, CD123/CD11c, CD94, CD4, CD8, and CD25/HLA-DR was performed. Cells were counted in both the epidermis and dermis over at least 2 mm of basal membrane length. + T cells. In the dermis, inflammatory activation is reflected by the influx of mature mDCs and pDCs, NK cells, and T cells, suggesting that the cellular immune response on viral HPV infection occurs in the dermis of VIN patients. [Cancer Res 2008;68(16):6617-22]

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“…Since HPV infects stratified epithelia of the skin and mucosa, it is thought that HPV targets the different epithelial DC subsets (DCs and Langerhans Cells (LCs)) to escape immune surveillance. HPV infection decreases both DC and LC numbers in HPV lesions and blood (Giannini et al, 2002;Lee et al, 2006), inhibits LC activation and migration (Fausch et al, 2002(Fausch et al, , 2005Guess and McCance, 2005) and induces the influx of plasmacytoid DCs into the cervical lesions (Bontkes et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Binding of human papilloma virus L1 virus-like particles to dendritic cells is mediated through heparan sulfates and induces immune activation

et al. 2008

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Plasmacytoid dendritic cells are present in cervical carcinoma and become activated by human papillomavirus type 16 virus-like particles

Cited by 43 publications

References 20 publications

Breast Cancer Cell–Derived GM-CSF Licenses Regulatory Th2 Induction by Plasmacytoid Predendritic Cells in Aggressive Disease Subtypes

Breast Cancer Cell–Derived GM-CSF Licenses Regulatory Th2 Induction by Plasmacytoid Predendritic Cells in Aggressive Disease Subtypes

Disturbed Patterns of Immunocompetent Cells in Usual-Type Vulvar Intraepithelial Neoplasia

Binding of human papilloma virus L1 virus-like particles to dendritic cells is mediated through heparan sulfates and induces immune activation

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