Evidence map›Paper›PMID 21178115›Full record

ArticleJournal of leukocyte biology2011

Nitric oxide controls an inflammatory-like Ly6C(hi)PDCA1+ DC subset that regulates Th1 immune responses.

Daniela Giordano, Chang Li, Mehul S Suthar, Kevin E Draves, Daphne Y Ma, Michael Gale, Edward A Clark

Abstract read
In one paragraph

Article in Journal of leukocyte biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Type I IFN Sensing by cDCs and CD4Molecular therapy : the journal of the American Society of Gene Therapy · 2020
    Article
  9. Article
  10. Article
  11. Review
  12. Regulation of iNOS on Immune Cells and Its Role in Diseases.International journal of molecular sciences · 2018
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Daniela GiordanoDepartment of Immunology, University of Washington, Box 357330, 1959 N.E. Pacific St., Seattle, WA 98195, USA. giordano@u.washington.edu
Chang Li
Mehul S Suthar
Kevin E Draves
Daphne Y Ma
Michael Gale
Edward A Clark

Funding

West Nile Virus and host control of innate defensesU19AI083019 · NIAID · UNIVERSITY OF WASHINGTON · PI CLARK, EDWARD A · 2009 to 2018
$22.5M
Programming protective immunity by targeting antigens to the CD180 receptorR01AI052203 · NIAID · UNIVERSITY OF WASHINGTON · PI FULLER, DEBORAH H. · 2003 to 2019
$6.3M
FDRC1 AND FOLLICULAR DENDRITIC CELL SIGNALING PATHWAYSR37AI044257 · NIAID · UNIVERSITY OF WASHINGTON · PI CLARK, EDWARD A · 2004 to 2013
$4.0M
Role of B cell activating factor (BAFF) in B cell responses and autoimmunityR01AI044257 · NIAID · UNIVERSITY OF WASHINGTON · PI GILTIAY, NATALIA V · 1999 to 2020
$3.7M
The host response to West Nile VirusR21AI057568 · NIAID · UNIVERSITY OF WASHINGTON · PI GALE, MICHAEL J · 2005 to 2006
$424k
NIAID NIH HHS AI44257NIAID NIH HHS AI52203NIAID NIH HHS AI57568NIAID NIH HHS AI83019NIAID NIH HHS R01 AI044257NIAID NIH HHS R01 AI052203NIAID NIH HHS R21 AI057568NIAID NIH HHS R37 AI044257NIAID NIH HHS U19 AI083019
6 · The paper itself

Abstract

Using NOS2 KO mice, we investigated the hypothesis that NO modulation of BM-DC contributes to the NO-mediated control of Th1 immune responses. BM-DCs from NOS2 KO mice, compared with WT BM-DCs, have enhanced survival and responsiveness to TLR agonists, develop more Ly6C(hi)PDCA1(+) DCs that resemble inflammatory DCs and produce high levels of inflammatory cytokines. Also, compared with WT-infected mice, NOS2 KO mice infected with WNV showed enhanced expansion of a similar inflammatory Ly6C(hi)PDCA1(+) DC subset. Furthermore, in contrast to WT DCs, OVA-loaded NOS2 KO BM-DCs promoted increased IFN-γ production by OTII CD4(+) T cells in vitro and when adoptively transferred in vivo. The addition of a NO donor to NOS2 KO BM-DCs prior to OTII T cells priming in vivo was sufficient to revert Th1 immune responses to levels induced by WT BM-DCs. Thus, autocrine NO effects on maturation of inflammatory DCs and on DC programming of T cells may contribute to the protective role of NO in autoimmune diseases and infections. Regulating NO levels may be a useful tool to shape beneficial immune responses for DC-based immunotherapy.

Indexed as

AnimalsAntigens, LyAntigens, SurfaceApoptosis Regulatory ProteinsB7-2 AntigenBiomarkersCD4-Positive T-LymphocytesCell ProliferationCells, CulturedCell SurvivalCytokinesDendritic CellsDown-RegulationEpitopesImmunityInflammationAntigens, LyAntigens, SurfaceApoptosis Regulatory ProteinsB7-2 AntigenBiomarkersCytokinesEpitopesInflammation MediatorsInterferon-gammaLy-6C antigen, mouseNitric OxideNitric Oxide Synthase Type IINos2 protein, mousePdcd1 protein, mouseProgrammed Cell Death 1 ReceptorToll-Like Receptors

Identifiers

PMID21178115
PMCPMC3040463

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.