Here's how NCBI.NLM.NIH.GOV makes money* and how much!

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NCBI . NLM . NIH . GOV {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Ncbi.nlm.nih.gov Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Social Networks
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. Hosting Providers
  14. CDN Services

We began analyzing https://pmc.ncbi.nlm.nih.gov/articles/PMC3163735/, but it redirected us to https://pmc.ncbi.nlm.nih.gov/articles/PMC3163735/. The analysis below is for the second page.

Title[redir]:
T helper 17 cell heterogeneity and pathogenicity in autoimmune disease - PMC
Description:
Th17 cells have been proposed to represent a new CD4+ T cell lineage important for host defense against fungi and extracellular bacteria, and the development of autoimmune diseases. Precisely how these cells arise has been the subject of some debate ...

Matching Content Categories {📚}

  • Science
  • Education
  • Law & Government

Content Management System {📝}

What CMS is ncbi.nlm.nih.gov built with?

Custom-built

No common CMS systems were detected on Ncbi.nlm.nih.gov, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of ncbi.nlm.nih.gov audience?

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


Based on our best estimate, this website will receive around 6,398,976 visitors per month in the current month.

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How Does Ncbi.nlm.nih.gov Make Money? {💸}

We can't tell how the site generates income.

Not every website is profit-driven; some are created to spread information or serve as an online presence. Websites can be made for many reasons. This could be one of them. Ncbi.nlm.nih.gov could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {🔍}

doi, cells, pubmed, google, scholar, pmc, article, free, tgfβ, differentiation, stat, cell, immunol, autoimmune, human, nat, disease, production, development, mice, factors, interleukin, transcription, ifnγ, immunity, helper, nature, autoimmunity, jimmuni, expression, med, lineage, signaling, eae, multiple, inflammatory, express, vivo, tbet, mouse, receptor, rev, cytokine, gene, factor, regulatory, exp, jem, diseases, ilproducing,

Topics {✒️}

transforming growth factor-beta interferon-gamma-expressing th17 cells therapeutics targeting il-12/il-23p40 genome-wide association study genome-wide association defines pmc beta search central nervous system apparent species-specific differences tgf-β-induced th17 cells tgf-beta indirectly favors nod/scid recipient mice pure il-17+ifn-γ− cells genome-wide association studies delayed-type hypersensitivity reactions relapsing-remitting multiple sclerosis phenotype-defining th17 genes readily produce ifn-γ ankylosing spondylitis identifies il-12p35 subunit developed cell-derived tgf-β readily express ifn-γ th17-driven inflammatory disease serum-free medium preventing runx1-mediated activation tgf-β acts indirectly dominant-negative mutations received tgf-β signals tgf-β1-independent manner [69] cell-mediated inflammatory autoimmunity ifn-γ double producers block tgf-β signaling induce il-23r expression genome-wide scale [89] tgf-beta-mediated regulation anti-p40 therapy tgf-β-induced cells transcription factor binding il-6-induced th17 cells hyper-ige syndrome [40–43] concluding remarks gene-microarray analysis hyper-ige syndrome ror nuclear receptors transcription factor gene selectively produced il-17 il-17-promoting cytokines il-6 nf-kappab pathways il-23-generated th17 cells il-17+ifn-γ− cells il-2–stat5 acting primarily

Questions {❓}

  • Does deletion of TGF-β impair Th17 differentiation because Th1 differentiation is exacerbated?
  • So, what are the initiating factors that induced receptor expression and first specify Th17 fate commitment?
  • This raises the question is TGF-β really important because it provides an obligate instructive signal to cells to become IL-17 producers or is TGF-β primarily limiting production of other cytokines, which in turn indirectly attenuate EAE?
  • What is the mechanism by which STAT3 participates in the development of this subset of cells?

Social Networks {👍}(6)

External Links {🔗}(226)

Analytics and Tracking {📊}

  • Google Analytics
  • Google Analytics 4
  • Google Tag Manager

Libraries {📚}

  • jQuery
  • jQuery module (jquery-3.6.0)
  • Zoom.js

Emails and Hosting {✉️}

Mail Servers:

  • nihcesxway.hub.nih.gov
  • nihcesxway2.hub.nih.gov
  • nihcesxway3.hub.nih.gov
  • nihcesxway4.hub.nih.gov
  • nihcesxway5.hub.nih.gov

Name Servers:

  • dns1-ncbi.ncbi.nlm.nih.gov
  • dns2-ncbi.ncbi.nlm.nih.gov
  • lhcns1.nlm.nih.gov
  • lhcns2.nlm.nih.gov

CDN Services {📦}

  • Ncbi

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