ReviewNature genetics2026
A systems perspective on monoallelic inborn errors of immunity.
Review in Nature genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The genetic architecture of inborn errors of immunity continues to grow in complexity, exposing the limitations of variant-centric concepts that have long shaped the field. While complete loss-of-function genotypes have been instrumental in defining essential gene functions in human immunity and inflammation, they have also entrenched binary interpretations of causality that fail to account for pleiotropy, variable expressivity and incomplete penetrance-especially in monoallelic disease. Monoallelic variants often perturb signaling rather than abolishing it. The integration of these perturbations into molecular and cellular systems, and eventually immune circuits, governs phenotypic expression. Here, we revisit and extend classic concepts of genetic dominance and genetic pleiotropy and suggest that these are not sole properties of alleles but emerge from the complex and dynamic behavior of molecular, cellular and immune systems to buffer genetic variance.
Identifiers
42901985What OpenQuestion holds
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.