combinatorial cytokine code generates antiviral state in dendritic cells

Clicks: 8
ID: 254982
2014
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #642 of 644 articles by views in sudebno-meditsinskaia ekspertiza

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 644 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
The physiological function of the immune system and the response to therapeutic immunomodulators may be sensitive to combinatorial cytokine micro-environments that shape the responses of specific immune cells. Previous work shows that paracrine cytokines released by virus-infected human dendritic cells (DC) can dictate the maturation state of naïve DCs. To understand the effects of paracrine signaling, we systematically studied the effects of combinations cytokines in this complex mixture in generating an antiviral state. After naïve DCs were exposed to either IFNβ or to paracrine signaling released by DCs infected by Newcastle Disease Virus (NDV), microarray analysis revealed a large number of genes that were differently regulated by the DC-secreted paracrine signaling. In order to identify the cytokine mechanisms involved, we identified 20 cytokines secreted by NDV infected DCs for which the corresponding receptor gene is expressed in naïve DCs. By exposing cells to all combinations of 19 cytokines (leave-one-out studies) we identified 5 cytokines (IFNβ, TNFα, IL-1β, TNFSF15 and IL28) as candidates for regulating DC maturation markers. Subsequent experiments identified IFNβ, TNFα and IL1β as the major contributors to this antiviral state. This finding was supported by infection studies in vitro, by T cell activation studies and by in vivo infection studies in mouse. Combination of cytokines can cause response states in DCs that differ from those achieved by the individual cytokines alone. These results suggest that the cytokine microenvironment may act via a combinatorial code to direct the response state of specific immune cells. Further elucidation of this code may provide insight into responses to infection and neoplasia as well as guide the development of combinatorial cytokine immunomodulation for infectious, autoimmune and immunosurveillance-related diseases.
Reference Key
hartmann2014frontierscombinatorial Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Boris Michael Hartmann;Nada eMarjanovic;German eNudelman;Thomas M. Moran;Stuart C. Sealfon
Journal sudebno-meditsinskaia ekspertiza
Year 2014
DOI
10.3389/fimmu.2014.00073
URL
http://journal.frontiersin.org/Journal/10.3389/fimmu.2014.00073/full
Keywords
allergy

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.