ReviewFrontiers in immunology2026
HLA polymorphism in neuroimmune diseases: linking antigen presentation to neuroinflammatory programs.
Review 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human leukocyte antigen (HLA) polymorphism shapes antigen presentation and susceptibility to immune-mediated disease. In neuroimmune disorders, a central question is how HLA-dependent antigen visibility becomes disease-specific immunity and tissue injury. In this Review, we integrate genetic, molecular, cellular, and clinical evidence across multiple sclerosis (MS), neuromyelitis optica spectrum disorder, Guillain-Barré syndrome, narcolepsy, autoimmune encephalitis, and myasthenia gravis. The HLA-DR15-MS axis is the most mechanistically resolved example, linking allele-specific peptide display to autoreactive T-cell repertoires and convergent Epstein-Barr virus-related immune pathways. In other disorders, this upstream principle operates through distinct effectors, target tissues, molecular subtypes, and ancestral contexts, while causal peptide-receptor complexes often remain unresolved. We therefore separate association strength from mechanistic resolution and position glial activation and tissue injury mainly as downstream, context-dependent processes. This evidence-bounded synthesis identifies where HLA mechanisms are established, suggestive, or still inferred from association.
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.