Toll-Like Receptors in Human Papillomavirus Infection

Review

DOI: 10.1007/s00005-013-0220-7

Cite this article as:
Zhou, Q., Zhu, K. & Cheng, H. Arch. Immunol. Ther. Exp. (2013) 61: 203. doi:10.1007/s00005-013-0220-7

Abstract

Infection with human papillomaviruses (HPVs) often causes cutaneous benign lesions, cervical cancer, and a number of other tumors. The mechanisms of host immune system to prevent and control HPV infection still remain poorly understood. Toll-like receptors (TLRs) are specific pattern recognition molecules that bind to microbial components to trigger innate immunity and direct adaptive immunity in the face of immunological danger. TLRs have been established to play an essential role in sensing and initiating antiviral immune responses. Recent accumulating evidence demonstrated that HPVs modulate TLR expression and interfere with TLR signaling pathways, leading to persistent viral infection and carcinogenesis. This review summarizes current knowledge on the roles of TLR during HPV infection, focusing on TLR recognition, modulation of TLR expression and signaling, regulatory receptors involved in TLR signaling, and cross-talk of TLRs with antimicrobial peptides. Immunotherapeutic strategies based on TLR agonists have emerged to be one of the novel promising avenues in treatment of HPV-associated diseases in the future.

Keywords

TLR HPV Innate immunity Adaptive immunity TLR agonist 

Abbreviations

AP-1

Activator protein-1

AMPs

Antimicrobial peptides

BCR

B cell receptor

CA

Condyloma acuminatum

CIN

Cervical intraepithelial neoplasia

DC

Dendritic cell

DCIR

DC-immunoreceptor

FcεR

Fc receptor for IgE

GAG

Glycosaminoglycan

hBD

Human β-defensin

HPV

Human papillomavirus

IFN

Interferon

IKK

IκB kinase kinase

IL

Interleukin

IRAK

IL-1 receptor-associated kinase

IRF

IFN regulatory factor

ITAM

Immunoreceptor tyrosine-based activation motif

LC

Langerhans cell

MAPKs

Mitogen-activated protein kinases

mDC

Myeloid dendritic cell

mdDC

Monocyte-derived DC

MyD88

Myeloid-differentiation primary-response gene 88

NF-κB

Nuclear factor-kappa B

NK

Natural killer

PAMPs

Pathogen-associated molecular patterns

pDC

Plasmacytoid DC

poly I:C

Polyinosinic-polycytidylic acid

RIP1

Receptor-interacting protein kinase 1

Siglec-H

Sialic-acid-binding-immunoglobulin-like-lectin H

siRNA

Short interfering RNA

TAK1

TGF-β-activated kinase 1

TBK

Tank-binding kinase

TIR

Toll/interleukin-1 receptor

TIRAP

TIR domain-containing adaptor protein

TLR

Toll-like receptor

TRAM

TRIF-related adaptor molecule

TRAF

Tumor necrosis factor receptor-associated factor

Treg

Regulatory T cells

TRIF

TIR domain-containing adaptor protein inducing IFNβ

VLPs

Virus-like particles

Copyright information

© L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2013

Authors and Affiliations

  1. 1.Department of Dermatology, Sir Run Run Shaw Hospital, School of MedicineZhejiang UniversityHangzhouPeople’s Republic of China

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