A model of impaired Langerhans cell maturation associated with HPV induced epithelial hyperplasia

Tuong, Zewen Kelvin; Lukowski, Samuel W.; Nguyen, Quan; Chandra, Janin; Zhou, Chenhao; Gillinder, Kevin R.; Bashaw, Abate Assefa; Ferdinand, John R.; Stewart, Benjamin; Teoh, Siok Min; Hanson, Sarah; Devitt, Katharina; Clatworthy, Menna R.; Powell, Joseph E.; Frazer, Ian H.

doi:10.1016/j.isci.2021.103326

Cited by 10 publications

(4 citation statements)

References 85 publications

(126 reference statements)

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“…Reduced E-cadherin levels caused by E7 protein also suggested the blockade of LCs adhesion with infected keratinocytes ( 56 , 57 ), negatively affecting antigen uptake in epidermis after HPV infections. Moreover, the LC-keratinocyte crosstalk was dysregulated including decreased expression of interleukin-34 and depletion of immune-stimulatory LCs ( 58 ).…”

Section: Suppressed Lcs Activities Caused By Cervical Hpv Infectionsmentioning

confidence: 99%

The association of cervicovaginal Langerhans cells with clearance of human papillomavirus

Dai

Gui

et al. 2022

Front. Immunol.

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Human papillomavirus (HPV) clearance is important in eliminating cervical cancer which contributes to high morbidity and mortality in women. Nevertheless, it remains largely unknown about key players in clearing pre-existing HPV infections. HPV antigens can be detected by the most important cervical antigen-presenting cells (Langerhans cells, LCs), of which the activities can be affected by cervicovaginal microbiota. In this review, we first introduce persistent HPV infections and then describe HPV-suppressed LCs activities, including but not limited to antigen uptake and presentation. Given specific transcriptional profiling of LCs in cervical epithelium, we also discuss the impact of cervicovaginal microbiota on LCs activation as well as the promise of exploring key microbial players in activating LCs and HPV-specific cellular immunity.

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Section: Suppressed Lcs Activities Caused By Cervical Hpv Infectionsmentioning

confidence: 99%

The association of cervicovaginal Langerhans cells with clearance of human papillomavirus

Dai

Gui

et al. 2022

Front. Immunol.

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“…The recognition of MHC I by CD8 + cells is a key step in the immune cytotoxicity of CD8 + CTLs. CD4 + T cells can also produce immunity against HPV infection, The immune effect may be activated after MHC II molecules are recognized by CD4 + T cells [ 39 ]. Compared with the HPV infection group, CT/HPV coinfection further downregulated the expression of MHC I and MHC II molecules on the LC surface and reduced the CD4 + and CD8 + CTL subsets, thus inhibiting cell-mediated immunity and leading to persistent HPV infection.…”

Section: Discussionmentioning

confidence: 99%

Chlamydia trachomatis enhances HPV persistence through immune modulation

Lu,

Wu,

Wang

et al. 2024

BMC Infect Dis

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Chlamydia trachomatis (CT) is the most common sexually transmitted infections globally, and CT infection can enhance HPV persistence. Epidemiological analysis has shown that patients with CT/HPV coinfection have a higher risk of developing cervical cancer and exhibit more rapid progression to cervical cancer than patients with HPV infection alone. However, the mechanism has not been fully elucidated. Here, we report that CT infection supports HPV persistence by further suppressing the functions of Langerhans cells (LCs); in particular, CT further activates the PI3K pathway and inhibits the MAPK pathways in LCs, and these pathways are frequently involved in the regulation of immune responses. CT/HPV coinfection also impairs LC functions by reducing the antigen-presenting ability and density of LCs. Moreover, CT/HPV coinfection can alter T-cell subsets, resulting in fewer CD4 + and CD8 + T cells and more infiltrating Tregs. Moreover, CT/HPV coinfection decreases the CD4 + /CD8 + T cell ratio to below 1, coinfection also induces greater T lymphocytes’ apoptosis than HPV infection, thus impairing cell-mediated immunity and accelerating the progress to cervical cancer.

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“…Major histocompatibility complex (MHC) presentation of HPV antigen required to generate useful cell‐mediated immunity during the early stages of infection is largely dependent on Langerhans cells, 10 or cross‐presentation during later stages of epithelial cell differentiation and viral shedding. Moreover, downregulation of antigen presentation by inhibition of MHC or perturbation of a normal cellular life cycle means that while disease may be present in 20–50% of the general population 11 at any one time, these responses are characteristically limited 12 .…”

Section: Cd4+ T‐lymphocyte Responses During Natural Hpv Infectionmentioning

confidence: 99%

The crossroads: divergent roles of virus‐specific CD4⁺ T lymphocytes in determining the outcome for human papillomavirus infection

Bockel

Kelleher

2023

Immunol Cell Biol

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Despite the widespread availability of effective prophylactic vaccines to prevent human papillomavirus (HPV) infection, HPV remains a major health burden. For health care systems in countries with the capacity for vaccine roll out, incomplete strategies result in citizens with naturally occurring infection, who are at an a posteriori risk of HPV‐driven disease. Genital HPV infection is the most common sexually transmitted virus globally. Those classified as high‐risk HPV strains are more likely to generate persistent disease. Within this group, HPV16 and 18 are the most prevalent and likely to induce persistent high‐grade squamous intraepithelial neoplasia; neoplasia is a large step toward cancerous growth known as a squamous cell carcinoma which contribute to all cervical, 70% of oropharyngeal, 78% of vaginal and 88% of anal cancers. This review will illuminate the relevance of CD4+ T lymphocytes in determining the outcome of papillomavirus infection from the perspective of oropharyngeal and anogenital HPV‐driven disease in the immune competent and immunocompromised. The focus is on recent investigations for this “silent” pandemic among current global health crises that should not be forgotten. Informing effective strategies that control viral infection through naturally acquired or induced immunity will identify aspects of scientific and clinical practice that may improve outcome.

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A model of impaired Langerhans cell maturation associated with HPV induced epithelial hyperplasia

Cited by 10 publications

References 85 publications

The association of cervicovaginal Langerhans cells with clearance of human papillomavirus

The association of cervicovaginal Langerhans cells with clearance of human papillomavirus

Chlamydia trachomatis enhances HPV persistence through immune modulation

The crossroads: divergent roles of virus‐specific CD4⁺ T lymphocytes in determining the outcome for human papillomavirus infection

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A model of impaired Langerhans cell maturation associated with HPV induced epithelial hyperplasia

Cited by 10 publications

References 85 publications

The association of cervicovaginal Langerhans cells with clearance of human papillomavirus

The association of cervicovaginal Langerhans cells with clearance of human papillomavirus

Chlamydia trachomatis enhances HPV persistence through immune modulation

The crossroads: divergent roles of virus‐specific CD4+ T lymphocytes in determining the outcome for human papillomavirus infection

Contact Info

Product

Resources

About

The crossroads: divergent roles of virus‐specific CD4⁺ T lymphocytes in determining the outcome for human papillomavirus infection