Evidence map›Paper›PMID 39937858›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2025

Engineered immunological niche directs therapeutic development in models of progressive multiple sclerosis.

Laila M Rad, Kevin R Hughes, Sydney N Wheeler, Joseph T Decker, Sophia M Orbach, Angelica Galvan, Jasmine Thornhill, Kate V Griffin, Hamza Turkistani, Russell R Urie and 3 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Antigen-conjugated scaffolds enable sustained delivery of antigen and enrichment of antigen-specific T-cells.Journal of controlled release : official journal of the Controlled Release Society · 2026
    Article
  4. Review
  5. 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

13 authors.

Laila M Rad *Department of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.ORCID 0000-0001-7965-7272
Kevin R Hughes *Department of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.ORCID 0000-0002-1706-2799
Sydney N WheelerDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.ORCID 0009-0008-8221-5449
Joseph T DeckerDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.ORCID 0000-0001-7914-4741
Sophia M OrbachDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.
Angelica GalvanDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.ORCID 0000-0002-7616-4760
Jasmine ThornhillDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.
Kate V GriffinDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.ORCID 0000-0002-8644-7780
Hamza TurkistaniDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.
Russell R UrieDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.
David N IraniDepartment of Neurology, University of Michigan Medical School, Ann Arbor, MI 48109.ORCID 0000-0002-3634-1742
Lonnie D SheaDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.
Aaron H MorrisDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.ORCID 0000-0002-4680-2493

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Eric R. Fearon · 1988 to 2026
$178.2M
Tissue Engineering and RegenerationT32DE007057 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAVID H. KOHN · 1985 to 2026
$17.3M
Postdoc Stipend Supplement: Developmental Origins of Metabolic Disorders T32T32DK071212 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAVID P OLSON, Kanakadurga Singer · 2005 to 2026
$5.4M
NPs disguised as apoptotic debris for immune toleranceR01AI155678 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI STEPHEN D MILLER, Lonnie D Shea · 2020 to 2026
$4.7M
Identifying intercellular circuits driving cell phenotypes within a nicheR01CA243916 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JERUSS, JACQUELINE SARA, SHEA, LONNIE D · 2019 to 2023
$2.3M
Tissue engineering tools for monitoring the cellular and molecular response to therapyR01CA272940 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JACQUELINE SARA JERUSS, Lonnie D Shea · 2023 to 2026
$1.7M
Supplement to Immunological Niches and Noninvasive Biosensors for Autoimmune MonitoringR00EB028840 · NIBIB · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MORRIS, AARON HARVEY · 2022 to 2025
$912k
HHS | NIH | National Institute of Biomedical Imaging and Bioengineering (NIBIB) R00EB028840HHS | NIH (NIH) 1R01AI155678HHS | NIH (NIH) 1R01CA243916HHS | NIH (NIH) R01CA272940NCI NIH HHS P30 CA046592NCI NIH HHS R01 CA243916NCI NIH HHS R01 CA272940NIAID NIH HHS R01 AI155678NIBIB NIH HHS R00 EB028840NIDCR NIH HHS T32 DE007057NIDDK NIH HHS T32 DK071212
6 · The paper itself

Abstract

Primary progressive multiple sclerosis (MS) is a demyelinating autoimmune disease with only a single class of FDA-approved treatment, B cell depletion. Novel treatments could emerge from a deeper understanding of the interplay between multiple cell types within diseased tissue throughout progression. We initially describe an engineered biomaterial-based immunological niche (IN) as a surrogate for diseased tissue to investigate immune cell function and phenotype dynamics throughout a chronic progressive mouse model of MS. Using these niches, we identify an array of dysregulated CC chemokine signaling as potential targets. We then develop antigen-loaded nanoparticles that reduce CC chemokine signaling, while delivering antigen. These nanoparticles serve as an antigen-specific treatment, and a single injection reduces disease burden, even if administered after symptomatic disease onset. This report demonstrates proof of principle of a biomaterial scaffold as a diseased tissue surrogate that can monitor immune function, identify potential drug targets, and guide the development of a therapeutic.

Indexed as

Multiple SclerosisMultiple Sclerosis, Chronic ProgressiveAnimalsBiocompatible MaterialsDisease Models, AnimalFemaleHumansMiceMice, Inbred C57BLNanoparticlesBiocompatible Materialsautoimmunitybiomaterialsimmunoengineeringmultiple sclerosisregenerative medicine

Identifiers

PMID39937858
PMCPMC11848328

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.