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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
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  6. Keywords
  7. Topics
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We are analyzing https://link.springer.com/article/10.1007/s10156-012-0485-5.

Title:
Immune responses against human papillomavirus (HPV) infection and evasion of host defense in cervical cancer | Journal of Infection and Chemotherapy
Description:
Human papillomavirus (HPV) is the most important etiological factor for cervical cancer. A recent study demonstrated that more than 20 HPV types were thought to be oncogenic for uterine cervical cancer. Notably, more than one-half of women show cervical HPV infections soon after their sexual debut, and about 90 % of such infections are cleared within 3 years. Immunity against HPV might be important for elimination of the virus. The innate immune responses involving macrophages, natural killer cells, and natural killer T cells may play a role in the first line of defense against HPV infection. In the second line of defense, adaptive immunity via cytotoxic T lymphocytes (CTLs) targeting HPV16 E2 and E6 proteins appears to eliminate cells infected with HPV16. However, HPV can evade host immune responses. First, HPV does not kill host cells during viral replication and therefore neither presents viral antigen nor induces inflammation. HPV16 E6 and E7 proteins downregulate the expression of type-1 interferons (IFNs) in host cells. The lack of co-stimulatory signals by inflammatory cytokines including IFNs during antigen recognition may induce immune tolerance rather than the appropriate responses. Moreover, HPV16 E5 protein downregulates the expression of HLA-class 1, and it facilitates evasion of CTL attack. These mechanisms of immune evasion may eventually support the establishment of persistent HPV infection, leading to the induction of cervical cancer. Considering such immunological events, prophylactic HPV16 and 18 vaccine appears to be the best way to prevent cervical cancer in women who are immunized in adolescence.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Health & Fitness
  • Education

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

The income method remains a mystery to us.

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Link.springer.com has a secret sauce for making money, but we can't detect it yet.

Keywords {🔍}

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Topics {✒️}

induce immune tolerance month download article/chapter hiroaki takagi & satoru makinoda immune evasion tumor necrosis factor-alpha t-cell proliferative responses human papilloma viruses haematopoietic stem-cell transplantation nitric oxide-dependent mechanisms escape immune recognition human immunodeficiency virus adaptive immunity foxp3-expressing regulatory full article pdf previous viral encounter human papillomavirus genomes kill host cells facilitates evasion human papillomavirus infection presents viral antigen human papillomavirus types immune responses privacy choices/manage cookies squamous cell carcinomas immune suppression hausen van der logt targeting hpv16 e2 de villiers em hiv-positive men e6 proteins appears e7 proteins downregulate evasion curr opin oncol cervical intraepithelial lesions recent study demonstrated sex transm dis eliminate cells infected reduced cytotoxic activity chemotherapy toshiyuki sasagawa cervical intraepithelial neoplasia hormone replacement therapy rincon-orozco mcp-1 chemokine transcription del toro-arreola sanchez-hernandez pe ramirez-dueñas mg increased secretion patterns phase ii trial azar kk

Schema {🗺️}

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         headline:Immune responses against human papillomavirus (HPV) infection and evasion of host defense in cervical cancer
         description:Human papillomavirus (HPV) is the most important etiological factor for cervical cancer. A recent study demonstrated that more than 20 HPV types were thought to be oncogenic for uterine cervical cancer. Notably, more than one-half of women show cervical HPV infections soon after their sexual debut, and about 90 % of such infections are cleared within 3 years. Immunity against HPV might be important for elimination of the virus. The innate immune responses involving macrophages, natural killer cells, and natural killer T cells may play a role in the first line of defense against HPV infection. In the second line of defense, adaptive immunity via cytotoxic T lymphocytes (CTLs) targeting HPV16 E2 and E6 proteins appears to eliminate cells infected with HPV16. However, HPV can evade host immune responses. First, HPV does not kill host cells during viral replication and therefore neither presents viral antigen nor induces inflammation. HPV16 E6 and E7 proteins downregulate the expression of type-1 interferons (IFNs) in host cells. The lack of co-stimulatory signals by inflammatory cytokines including IFNs during antigen recognition may induce immune tolerance rather than the appropriate responses. Moreover, HPV16 E5 protein downregulates the expression of HLA-class 1, and it facilitates evasion of CTL attack. These mechanisms of immune evasion may eventually support the establishment of persistent HPV infection, leading to the induction of cervical cancer. Considering such immunological events, prophylactic HPV16 and 18 vaccine appears to be the best way to prevent cervical cancer in women who are immunized in adolescence.
         datePublished:2012-11-03T00:00:00Z
         dateModified:2012-11-03T00:00:00Z
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            Infectious Diseases
            Medical Microbiology
            Virology
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      headline:Immune responses against human papillomavirus (HPV) infection and evasion of host defense in cervical cancer
      description:Human papillomavirus (HPV) is the most important etiological factor for cervical cancer. A recent study demonstrated that more than 20 HPV types were thought to be oncogenic for uterine cervical cancer. Notably, more than one-half of women show cervical HPV infections soon after their sexual debut, and about 90 % of such infections are cleared within 3 years. Immunity against HPV might be important for elimination of the virus. The innate immune responses involving macrophages, natural killer cells, and natural killer T cells may play a role in the first line of defense against HPV infection. In the second line of defense, adaptive immunity via cytotoxic T lymphocytes (CTLs) targeting HPV16 E2 and E6 proteins appears to eliminate cells infected with HPV16. However, HPV can evade host immune responses. First, HPV does not kill host cells during viral replication and therefore neither presents viral antigen nor induces inflammation. HPV16 E6 and E7 proteins downregulate the expression of type-1 interferons (IFNs) in host cells. The lack of co-stimulatory signals by inflammatory cytokines including IFNs during antigen recognition may induce immune tolerance rather than the appropriate responses. Moreover, HPV16 E5 protein downregulates the expression of HLA-class 1, and it facilitates evasion of CTL attack. These mechanisms of immune evasion may eventually support the establishment of persistent HPV infection, leading to the induction of cervical cancer. Considering such immunological events, prophylactic HPV16 and 18 vaccine appears to be the best way to prevent cervical cancer in women who are immunized in adolescence.
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      dateModified:2012-11-03T00:00:00Z
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         Human papillomavirus
         Cervical cancer
         Innate immunity
         Adaptive immunity
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         Immune tolerance
         Infectious Diseases
         Medical Microbiology
         Virology
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External Links {🔗}(144)

Analytics and Tracking {📊}

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Libraries {📚}

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  • Crossref

4.2s.