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Review
. 2015 Aug;22(8):850-7.
doi: 10.1128/CVI.00223-15. Epub 2015 Jun 10.

Early Defensive Mechanisms against Human Papillomavirus Infection

Andrea Moerman-Herzog  1 , Mayumi Nakagawa  2
Affiliations
Review

Early Defensive Mechanisms against Human Papillomavirus Infection

Andrea Moerman-Herzog et al. Clin Vaccine Immunol. 2015 Aug.

Abstract

Cervical cancer is the fourth most common cancer in women and is almost exclusively caused by human papillomavirus (HPV) infection VSports手机版. HPV is also frequently associated with other cancers arising from mucosal epithelium, including anal and oropharyngeal cancers, which are becoming more common in both men and women. Viral persistence and progression through precancerous lesion stages are prerequisites for HPV-associated cancer and reflect the inability of cell-mediated immune mechanisms to clear infections and eliminate abnormal cells in some individuals. Cell-mediated immune responses are initiated by innate pathogen sensing and subsequent secretion of soluble immune mediators and amplified by the recruitment and activation of effector T lymphocytes. This review discusses early defensive mechanisms of innate responders to natural HPV infection, their influence on response polarization, and the underappreciated role of keratinocytes in this process. .

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FIG 1
FIG 1
Activated KC amplify cell-mediated immune reactions. Resting KC express low surface levels of CD40 and ICAM-1, moderate levels of MHC-I, and high levels of IFN-γ receptor (IFN-γR) (82, 90, 91) (A). Activation of KC by IFN-γ secreted by NK cells or activated T lymphocytes (B) increases surface expression of MHC-I, MHC-II, CD40, and ICAM-1 (82, 83, 90–92) and induces expression of CXCL9, CXCL10, and CXCL11 (94), chemokines that attract activated Th1 cells (C). KC that present HPV antigens via MHC-II may interact with Th1 cells (D). Higher surface expression of ICAM-1 and CD40 improves adhesion and costimulation (82, 83, 91). Ligation of CD40 on KC by CD40 ligand on Th1 cells further increases ICAM-1 (83, 90) and stimulates further cytokine and chemokine expression (90–94) to activate and recruit additional immune cells (E).
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