ArticleVirchows Archiv : an international journal of pathology2025
Perforin-2 is overexpressed in Kikuchi-Fujimoto disease.
Article in Virchows Archiv : an international journal of pathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Late recurrence of Kikuchi-Fujimoto disease nine years after initial diagnosis: a case-based review.Clinical rheumatology · 2026Article
- Exploring Genetic Clues in Kikuchi-Fujimoto Disease: A Three-Generation Study.Pharmacogenomics and personalized medicine · 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kikuchi-Fujimoto disease (KFD) is a self-limited lymphadenopathy characterized by subcortical necrosis and paracortical proliferation of lymphocytes, histiocytes and plasmacytoid dendritic cells with abundant apoptosis. The etiology of KFD remains unknown. Perforin-2 is a highly conserved transmembrane molecule capable of forming pores following intercellular interaction with bacteria and erythrocytes. Perforin-2 is also essential for the activation of type I interferon-induced JAK/STAT signaling and elimination of virus infection. Herein, we hypothesized that perforin-2 or macrophage-expressed gene 1 (MPEG1) protein function is dysregulated in KFD, resulting in an exaggerated immune response, possibly following exposure to an unknown infectious agent. Twelve cases of KFD were the study group. We isolated total RNA from fixed, paraffin-embedded whole tissue sections. We also assessed primary human B-cells and 4 cases of reactive follicular hyperplasia as controls. Perforin-2 mRNA levels were assessed by quantitative real-time PCR (qRT-PCR). We found that perforin-2 mRNA expression was significantly upregulated in 11 of 12 (92%) KFD cases as compared with control samples. These results suggest that expression of perforin-2 is dramatically upregulated in KFD cases. Increased levels of perforin-2 likely explain the abundant apoptosis in KFD. These data also support the hypothesis that upregulation of perforin-2 may be part of the host immune reaction to an unknown infectious agent that is the trigger for KFD.
Indexed as
Identifiers
39915303What 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.