ArticleFrontiers in immunology2023
Single-cell transcriptomic analysis in two patients with rare systemic autoinflammatory diseases treated with anti-TNF therapy.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- Effectiveness of "tumor necrosis factor inhibitors" in monogenic hereditary recurrent fevers in children and adolescents: a systematic review.Frontiers in immunology · 2025Pooled it
- sc-MULTI-omics approach in nano-rare diseases: understanding the pathophysiological mechanism of Mulvihill-Smith Syndrome.Functional & integrative genomics · 2025Article
- SeuratExtend: streamlining single-cell RNA-seq analysis through an integrated and intuitive framework.GigaScience · 2025Article
- RNA Sequencing in Disease Diagnosis.Annual review of genomics and human genetics · 2024Review
- Identification of an anaplastic subtype of prostate cancer amenable to therapies targeting SP1 or translation elongation.Science advances · 2024Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic autoinflammatory diseases (SAIDs) are a group of rare diseases characterized by recurrent or continuous inflammation, typically accompanied by genetic variants. Good responses to anti-TNF therapy were observed in SAIDs patients. However, the mechanisms underlying the disease flare and the response to TNF blocking therapy have not been fully elucidated. Here, single-cell RNA sequencing technology was used to describe the transcriptomic profile of PBMCs and PMNs in two SAID patients both before and after anti-TNF treatment. Interferon responses were involved in the disease flare. After anti-TNF therapy, clinical symptoms were alleviated while TNF and IL-1 were unexpectedly increased, indicating that these inflammatory cytokines are not positively correlated with disease activity. Trajectory analysis showed that inhibition of macrophage differentiation, rather than reduction of the inflammatory cytokines, as the potential mechanism of anti-TNF treatment response in SAIDs.
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Registered trials
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