ArticleFrontiers in immunology2026
Cooperative control of IgA synthesis and secretion by MZB1 and the J chain.
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.
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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunoglobulin A (IgA) is the most abundantly produced antibody in mammals, with its secretory dimeric form playing a central role in maintaining intestinal homeostasis. Although the J chain is known to be essential for IgA transcytosis, its precise role in IgA biosynthesis and secretion is not fully understood. Here, using CRISPR/Cas9-edited J558 plasmacytoma cells, a mouse line that secretes IgA, we demonstrate that MZB1 and the J chain act sequentially to ensure proper IgA assembly. MZB1 stabilizes α-heavy chain-light chain complexes (HL complexes), thereby enabling their efficient association with the J chain, which subsequently drives rapid assembly into IgA dimers and higher-order polymers. Loss of MZB1 reduced the secretion of dimeric IgA, whereas J chain deficiency caused both excessive intracellular accumulation and secretion of HL complexes, while allowing the generation and secretion of limited amounts of monomeric IgA but completely abolishing dimer formation. Combined deficiency reproduced the additive defects of the single knockouts, confirming their cooperative function in a shared assembly pathway.
Indexed as
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.