Evidence map›Paper›PMID 42311689›Full record

ArticleFrontiers in immunology2026

Gene expression profiling of dendritic cell tolerance dysfunction in women with systemic lupus erythematosus.

Ana Laura Hernández-Ledesma, Evelia Lorena Coss-Navarrete, Sofia Salazar-Magaña, Diego Ramírez-Espinosa, Lizbet Tinajero-Nieto, Estefania Torres-Valdez, Angélica H Peña-Ayala, Guillermo Félix-Rodriguez, Gabriel Frontana-Vázquez, Jair Santiago García Sotelo and 7 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 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

17 authors.

Ana Laura Hernández-Ledesma *Laboratorio Internacional de Investigación sobre el Genoma Humano, Universidad Nacional Autónoma de México, Santiago de Querétaro, Mexico.
Evelia Lorena Coss-Navarrete *Laboratorio Internacional de Investigación sobre el Genoma Humano, Universidad Nacional Autónoma de México, Santiago de Querétaro, Mexico.
Sofia Salazar-MagañaLaboratorio Internacional de Investigación sobre el Genoma Humano, Universidad Nacional Autónoma de México, Santiago de Querétaro, Mexico.
Diego Ramírez-EspinosaLaboratorio Internacional de Investigación sobre el Genoma Humano, Universidad Nacional Autónoma de México, Santiago de Querétaro, Mexico.
Lizbet Tinajero-NietoHospital General Regional No. 1, IMSS, Santiago de Querétaro, Querétaro, Mexico.
Estefania Torres-ValdezHospital General Regional No. 2, IMSS, El Marqués, Querétaro, Mexico.
Angélica H Peña-AyalaHospital General Regional No. 1, IMSS, Santiago de Querétaro, Querétaro, Mexico.
Guillermo Félix-RodriguezHospital Star Médica Querétaro, Santiago de Querétaro, Querétaro, Mexico.
Gabriel Frontana-VázquezHospital General Regional No. 2, IMSS, El Marqués, Querétaro, Mexico.
Jair Santiago García SoteloLaboratorio Internacional de Investigación sobre el Genoma Humano, Universidad Nacional Autónoma de México, Santiago de Querétaro, Mexico.
Morgane Thomas-ChollierGenomiqueENS, Institut de Biologie de l'ENS (IBENS), Département de biologie, École normale supérieure, CNRS, INSERM, Université PSL, Paris, France.
Gosia TrynkaOpen Targets, Cambridge, United Kingdom.
Florencia RosettiDepartamento de Inmunología y Reumatología, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Ciudad de México, Mexico.
Selene L Fernandez-ValverdeSchool of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney, NSW, Australia.
María Gutiérrez-ArcelusDivision of Immunology, Boston Children's Hospital, Boston, MA, United States.
Deshiré Alpízar-RodríguezInstituto Nacional de Rehabilitación "Luis Guillermo Ibarra Ibarra", Ciudad de México, Mexico.
Alejandra Medina-RiveraLaboratorio Internacional de Investigación sobre el Genoma Humano, Universidad Nacional Autónoma de México, Santiago de Querétaro, Mexico.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Dendritic cells (DCs) are central regulators of immune tolerance, and disturbances in their phenotype and function contribute to the breakdown of self-tolerance in systemic lupus erythematosus (SLE). Tolerogenic DCs (tolDCs), which suppress autoreactive responses and promote peripheral tolerance, are a promising therapeutic focus in autoimmune diseases. Methods: Here, we analyzed the transcriptional profiles of Results: Interferon stimulated genes (ISGs) emerged as dominant markers across all cellular contexts, with monocytes exhibiting the most substantial enrichment; key ISGs (I Conclusion: Together, these findings suggest that interferon driven transcriptional rewiring, impaired IL-10 signaling, and aberrant lipid metabolic programming converge to compromise DCs tolerogenic capacity in SLE. This highlights key mechanistic pathways that could be targeted to restore immune tolerance and reduce chronic inflammation.

Indexed as

Dendritic CellsImmune ToleranceLupus Erythematosus, SystemicTranscriptomeAdultFemaleGene Expression ProfilingHumansLipid Metabolismdendritic cellsimmune regulationsystemic lupus erythematosustolerance inductiontranscriptomics

Identifiers

PMID42311689
PMCPMC13270180

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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.