Evidence map›Paper›PMID 33169522›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2021

Suppression of Rheumatoid Arthritis by Enhanced Lymph Node Trafficking of Engineered Interleukin-10 in Murine Models.

Eiji Yuba, Erica Budina, Kiyomitsu Katsumata, Ako Ishihara, Aslan Mansurov, Aaron T Alpar, Elyse A Watkins, Peyman Hosseinchi, Joseph W Reda, Abigail L Lauterbach and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

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  16. Influence ofInternational journal of molecular sciences · 2022
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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

16 authors at 3 institutions in 3 countries.

Eiji YubaUniversity of Chicago, Chicago, Illinois, and Osaka Prefecture University, Osaka, Japan.ORCID 0000-0003-4984-2113
Erica BudinaUniversity of Chicago, Chicago, Illinois, USA.
Kiyomitsu KatsumataUniversity of Chicago, Chicago, Illinois, USA.ORCID 0000-0002-7726-7892
Ako IshiharaUniversity of Chicago, Chicago, Illinois, USA.
Aslan MansurovUniversity of Chicago, Chicago, Illinois, USA.
Aaron T AlparUniversity of Chicago, Chicago, Illinois, USA.
Elyse A WatkinsUniversity of Chicago, Chicago, Illinois, USA.
Peyman HosseinchiUniversity of Chicago, Chicago, Illinois, USA.
Joseph W RedaUniversity of Chicago, Chicago, Illinois, USA.
Abigail L LauterbachUniversity of Chicago, Chicago, Illinois, USA.
Mindy NguyenUniversity of Chicago, Chicago, Illinois, USA.
Ani SolankiUniversity of Chicago, Chicago, Illinois, USA.
Takahiro KageyamaUniversity of Illinois at Chicago, Chicago, USA.
Melody A SwartzUniversity of Chicago, Chicago, Illinois, USA.
Jun IshiharaUniversity of Chicago, Chicago, Illinois, and Imperial College London, London, UK.
Jeffrey A HubbellUniversity of Chicago, Chicago, Illinois, USA.
University of Chicago · USOsaka Prefecture University · JPUniversity of Illinois Chicago · US

Funding

Paradoxical roles of tumor lymphangiogenesis on tumor immunity and implications for immunotherapy - Resubmission 01R01CA219304 · NCI · UNIVERSITY OF CHICAGO · PI SWARTZ, MELODY ANN · 2018 to 2022
$1.8M
NCI NIH HHS R01 CA219304
6 · The paper itself

Abstract

objectiveRheumatoid arthritis (RA) is a major autoimmune disease that causes synovitis and joint damage. Although clinical trials have been performed using interleukin-10 (IL-10), an antiinflammatory cytokine, as a potential treatment of RA, the therapeutic effects of IL-10 have been limited, potentially due to insufficient residence in lymphoid organs, where antigen recognition primarily occurs. This study was undertaken to engineer an IL-10-serum albumin (SA) fusion protein and evaluate its effects in 2 murine models of RA.

methodsSA-fused IL-10 (SA-IL-10) was recombinantly expressed. Mice with collagen antibody-induced arthritis (n = 4-7 per group) or collagen-induced arthritis (n = 9-15 per group) were injected intravenously with wild-type IL-10 or SA-IL-10, and the retention of SA-IL-10 in the lymph nodes (LNs), immune cell composition in the paws, and therapeutic effect of SA-IL-10 on mice with arthritis were assessed.

resultsSA fusion to IL-10 led to enhanced accumulation in the mouse LNs compared with unmodified IL-10. Intravenous SA-IL-10 treatment restored immune cell composition in the paws to a normal status, elevated the frequency of suppressive alternatively activated macrophages, reduced IL-17A levels in the paw-draining LN, and protected joint morphology. Intravenous SA-IL-10 treatment showed similar efficacy as treatment with an anti-tumor necrosis factor antibody. SA-IL-10 was equally effective when administered intravenously, locally, or subcutaneously, which is a benefit for clinical translation of this molecule.

conclusionSA fusion to IL-10 is a simple but effective engineering strategy for RA therapy and has potential for clinical translation.

Indexed as

AnimalsAntigen-Presenting CellsArthritis, ExperimentalArthritis, RheumatoidDisease Models, AnimalFootFoot JointsHindlimbHistocompatibility Antigens Class IInjections, IntravenousInterleukin-10Interleukin-17Interleukin-6Lymph NodesMacrophage ActivationMacrophagesFc receptor, neonatalHistocompatibility Antigens Class IIl17a protein, mouseInterleukin-10Interleukin-17Interleukin-6Receptors, FcRecombinant Fusion ProteinsSerum AlbuminTransforming Growth Factor betaTumor Necrosis Factor Inhibitors

Identifiers

PMID33169522
PMCPMC11095083
OpenAlexW3102911773

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.