Evidence map›Paper›PMID 41886078›Full record

ArticleImmunoHorizons2026

Direct contact with natural killer cells reprograms monocyte-derived dendritic cells into a tolerogenic phenotype.

Ammar J Alsheikh, Liang Chen, Daniel Korenfeld, Jason Tam, Suresh Patil, Hsi-Ju Wei, Jianing Li, Suju Zhong, Feng Dong, Terry Melim and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in ImmunoHorizons, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

18 authors.

Ammar J AlsheikhCambridge Research Center, AbbVie, 200 Sidney Street, Cambridge, MA, 02139, USA.ORCID 0000-0001-7125-0144
Liang ChenCambridge Research Center, AbbVie, 200 Sidney Street, Cambridge, MA, 02139, USA.
Daniel KorenfeldCambridge Research Center, AbbVie, 200 Sidney Street, Cambridge, MA, 02139, USA.
Jason TamCambridge Research Center, AbbVie, 200 Sidney Street, Cambridge, MA, 02139, USA.
Suresh PatilCambridge Research Center, AbbVie, 200 Sidney Street, Cambridge, MA, 02139, USA.
Hsi-Ju WeiCambridge Research Center, AbbVie, 200 Sidney Street, Cambridge, MA, 02139, USA.
Jianing LiCambridge Research Center, AbbVie, 200 Sidney Street, Cambridge, MA, 02139, USA.
Suju ZhongCambridge Research Center, AbbVie, 200 Sidney Street, Cambridge, MA, 02139, USA.
Feng DongCambridge Research Center, AbbVie, 200 Sidney Street, Cambridge, MA, 02139, USA.
Terry MelimAbbVie Bioresearch Center, AbbVie, 100 Research Drive, Worcester, MA, 01605, USA.
Karin OrsiAbbVie Bioresearch Center, AbbVie, 100 Research Drive, Worcester, MA, 01605, USA.
Samuel KarsenAbbVie Bioresearch Center, AbbVie, 100 Research Drive, Worcester, MA, 01605, USA.
Yingli YangAbbVie Bioresearch Center, AbbVie, 100 Research Drive, Worcester, MA, 01605, USA.
Susan WestmorelandAbbVie Bioresearch Center, AbbVie, 100 Research Drive, Worcester, MA, 01605, USA.
Aridaman PanditCambridge Research Center, AbbVie, 200 Sidney Street, Cambridge, MA, 02139, USA.
Kevin WhiteCambridge Research Center, AbbVie, 200 Sidney Street, Cambridge, MA, 02139, USA.
Timothy RadstakeCambridge Research Center, AbbVie, 200 Sidney Street, Cambridge, MA, 02139, USA.
Abel Suarez-FueyoCambridge Research Center, AbbVie, 200 Sidney Street, Cambridge, MA, 02139, USA.

Funding

AbbVie
6 · The paper itself

Abstract

Tissue-infiltrating monocyte-derived dendritic cells (DCs) and macrophages are key antigen-presenting cells promoting inflammation and tissue damage by releasing proinflammatory cytokines and strongly activating T cells. These antigen-presenting cells are prominent in inflamed tissues, including in conditions such as inflammatory bowel disease. Modulating the number or function of these cells presents an opportunity to mitigate inflammation and promote immune tolerance in inflammatory disorders. In this study, we comprehensively evaluate a novel approach to modulate these cell populations. First, we employ an antibody-mediated approach to selectively deplete inflammatory DCs while simultaneously reprogramming surviving cells toward a tolerogenic phenotype. Second, we utilize a natural killer-DC co-culture system to dissect molecular mechanisms of DC tolerance induction through integrated transcriptomic and epigenomic analysis, complemented by functional assays. We confirm that the generated DCs exhibit tolerogenic properties, marked by a reduced ability to induce allogenic T-cell activation, increased expression of regulatory mediators including IL-10 and IDO1, and decreased levels of co-stimulatory and activation markers such as CD11c, CD40, and CD44. Finally, using CRISPR knockout, we confirm the essential role of transcription factors IKZF1 and PU.1 in this process. Our findings advance the understanding of how epigenetic remodeling and transcription factor activity govern DC tolerance, and highlight promising therapeutic avenues for DC-targeted therapeutic approaches in inflammatory disorders.

Indexed as

Dendritic CellsImmune ToleranceKiller Cells, NaturalAnimalsCells, CulturedCoculture TechniquesHumansLymphocyte ActivationMonocytesPhenotypeProto-Oncogene ProteinsProto-Oncogene Protein Spi-1T-LymphocytesProto-Oncogene ProteinsProto-Oncogene Protein Spi-1autoimmunitydendritic cellnatural killer celltolerance

Identifiers

PMID41886078
PMCPMC13020354

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Registered trials

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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.