ReviewJournal of human immunity2026
Human inborn errors of the alternative NF-κB pathway.
Review 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 3 papers.
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
3 citing papers in PubMed.
- A Detrimental NFKB2 Missense Variant is Associated with Hypogammaglobulinemia.Journal of clinical immunology · 2026Article
- Toward a monogenic architecture of human infections: From 1996 to 2026.Journal of human immunity · 2026Review
- High risk of hypoxemic COVID-19 pneumonia in myasthenia gravis patients with type I IFN autoantibodies.medRxiv : the preprint server for health sciences · 2026Article
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
Abstract
Inborn errors of the "core" components of the alternative NF-κB pathway-NIK, IKK-α, RelB, and NF-κB2-underlie various T and/or B cell deficiencies, frequently associated with syndromic features, including ectodermal dysplasia and lymph node hypoplasia. Their impact on medullary thymic stromal cells (mTECs) also underlies the development of autoantibodies neutralizing type I interferons (IFNs), conferring a predisposition to severe viral diseases. Inborn errors of "upstream" ligands or surface receptors engaging this pathway affect secondary lymphoid organ organization (LTβR), B cell development and survival (BAFFR), T cell and antigen-presenting cell costimulation (CD40L/CD40), or osteoclast differentiation (RANK/RANKL). Finally, inborn errors of TRAF3, a negative "regulator" of this pathway, underlie immune dysregulation, infection, and lymphoproliferation. Various inborn errors of the human alternative NF-κB pathway have, thus, delineated the essential and redundant roles of its components in leukocytic and non-leukocytic cells.
Identifiers
What 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.