Evidence map›Paper›PMID 30656310›Full record

ArticleBiomaterials science2019

Engineering release kinetics with polyelectrolyte multilayers to modulate TLR signaling and promote immune tolerance.

Lisa H Tostanoski, Haleigh B Eppler, Boyan Xia, Xiangbin Zeng, Christopher M Jewell

Abstract read
In one paragraph

Article in Biomaterials science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 26% of its field
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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Structural immunotherapy: Harnessing chemical design to build powerful next-generation therapeutics.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. Review
  6. Review
  7. Biomaterial Strategies for Selective Immune Tolerance: Advances and Gaps.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Biomaterials as Tools to Decode Immunity.Advanced materials (Deerfield Beach, Fla.) · 2020
    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

5 authors at 2 institutions in 3 countries.

Lisa H TostanoskiFischell Department of Bioengineering, A. James Clark Hall, Room 5110, 8278 Paint Branch Drive, College Park, Maryland 20742, USA. cmjewell@umd.edu.
Haleigh B Eppler
Boyan Xia
Xiangbin Zeng
Christopher M Jewell
Park University · USUniversity of Maryland, Baltimore · US

Funding

Training Program in Cell & Molecular BiologyT32GM080201 · NIGMS · UNIV OF MARYLAND, COLLEGE PARK · PI DELWICHE, CHARLES F · 2009 to 2019
$1.6M
Harnessing biomaterials to study the link between local lymph node function and systemic toleranceR01EB026896 · NIBIB · UNIV OF MARYLAND, COLLEGE PARK · PI JEWELL, CHRISTOPHER M · 2018 to 2021
$1.5M
Tunable Assembly of Regulatory Immune Signals to Promote Myelin-specific ToleranceI01BX003690 · VA · BALTIMORE VA MEDICAL CENTER · PI Christopher M Jewell · 2017 to 2026
–
BLRD VA I01 BX003690NIBIB NIH HHS R01 EB026896NIGMS NIH HHS T32 GM080201
6 · The paper itself

Abstract

Autoimmune disorders, such as multiple sclerosis and type 1 diabetes, occur when immune cells fail to recognize "self" molecules. Recently, studies have revealed aberrant inflammatory signaling through pathogen sensing pathways, such as toll-like receptors (TLRs), during autoimmune disease. Therapeutic inhibition of these pathways might attenuate disease development, skewing disease-causing inflammatory cells towards cell types that promote tolerance. Delivering antagonistic ligands to a TLR upstream of an inflammatory signaling cascade, TLR9, has demonstrated exciting potential in a mouse model of MS; however, strategies that enable sustained delivery could reduce the need for repeated administration or enhance therapeutic efficacy. We hypothesized that GpG - an oligonucleotide TLR9 antagonist - which is inherently anionic, could be self-assembled into polyelectrolyte multilayers (PEMs) with a cationic, degradable poly(β-amino ester) (Poly1). We hypothesized that degradable Poly1/GpG PEMs could promote sustained release of GpG and modulate inflammatory immune cell functions. Here we demonstrate layer-by-layer assembly of degradable PEMs, as well as subsequent degradation and release of GpG. Following assembly and release, GpG maintains the ability to reduce dendritic cell activation and inflammatory cytokine secretion, restrain TLR9 signaling, and polarize myelin specific T cells towards regulatory phenotypes and functions in primarily immune cells. These results indicate that degradable PEMs may be able to promote tolerogenic immune function in the context of autoimmunity.

Indexed as

Immune ToleranceSignal TransductionAnimalsCell LineCytokinesDendritic CellsHumansKineticsMiceMice, Inbred C57BLMultiple SclerosisOligodeoxyribonucleotidesPhenotypePolyelectrolytesPolymersT-LymphocytesCytokinesGpG-oligonucleotideOligodeoxyribonucleotidespoly(beta-amino ester)PolyelectrolytesPolymersToll-Like Receptor 9

Identifiers

PMID30656310
PMCPMC6391195
OpenAlexW2910744014

What OpenQuestion holds

Textmetadata
LicenceTDM
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.