ArticleJournal of human immunity2026
Response to recombinant human granulocyte colony-stimulating factor in reticular dysgenesis.
Article in Journal of human immunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
Who cites it
1 citing paper in PubMed.
- Nationwide TREC/KREC-based newborn screening and clinical outcomes in Japan.Journal of human immunity · 2026Article
Corrections and comments
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reticular dysgenesis (RD) is characterized by severe combined immunodeficiency and agranulocytosis with hematopoietic stem cell transplantation (HSCT) being the only curative therapy. Severe neutropenia in RD is typically unresponsive to recombinant human granulocyte colony-stimulating factor (rhG-CSF). To delineate lineage-specific transcriptional responses and cellular heterogeneity induced by rhG-CSF, we integrated single-cell RNA sequencing from seven samples, including two RD patients (with and without rhG-CSF) and three pediatric controls. We identified a moderate increase in hematopoietic stem and progenitor cells (HSPCs) and common myeloid progenitor/granulocyte-monocyte progenitor fractions following rhG-CSF. Notably, B cell fractions increased after rhG-CSF, accompanied by enhanced maturation from common lymphoid progenitors to precursor B cells. In parallel, genes involved in B cell differentiation were markedly upregulated compared with untreated cells. It also modulated the HSPC compartment by markedly suppressing interferon-γ (IFNγ) signaling pathways. RhG-CSF administration before HSCT may benefit patients with RD by modestly increasing neutrophils and supporting infection control, while suppressing IFNγ signaling in HSPCs and potentially promoting B cell differentiation.
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Registered trials
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.