ArticleFrontiers in neurology
Autoreactive T cells and thymic atrophy pathway in thymic hyperplasia patients with myasthenia gravis.
Article in Frontiers in neurology. 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: T cells play a vital role in antigen presentation, immune tolerance imbalance, and secretion of pathogenic cytokines in the progression of Myasthenia Gravis (MG). Previous studies have founded that patients with thymic hyperplasia accompanied by MG exhibit autoreactive T cells in thymus that can recognize self-antigens at the neuromuscular junction (NMJ), leading to the destruction of acetylcholine receptors (AChR) and the appearance of muscle weakness. Furthermore, Thymic hyperplasia is associated with T-cell-related autoimmune diseases, and increased expression of WNT4 and FOXN1 are beneficial to the growth of thymic cells and the maintenance of the thymic microenvironment. Methods: The samples were obtained from surgical patients who met the criteria, and this study was ethically approved. We first measured the proportion of T cell subsets in the peripheral blood and thymus of thymic hyperplasia patients with and without myasthenia gravis. Then, we quantified the WNT4 and FOXN1 proteins in the thymus. Finally, we used the Pearson correlation test to analyze the correlation between autoreactive T cells and the thymic atrophy pathway. Results: Flow cytometry clarified that Th1 and Th17 cells were elevated in the peripheral blood and thymus of patients with MG (1.207 ± 1.444 and 3.788 ± 0.6920 in Th1, 7.683 ± 1.025 and 0.3127 ± 0.1936 in Th17). Western blotting revealed increased expression of key molecules in the thymic atrophy pathway, WNT4 and FOXN1, in the MG group. Additionally, the abnormal activation of the thymic atrophy pathway may be one of the causes of autoreactive T cell production. Conclusion: Our study has identified an increased number of Th1 and Th17 cells in the peripheral blood and thymus of patients with thymic hyperplasia associated MG. Quantitative analysis of proteins and RNA indicates that the expression of WNT4 and FOXN1 is upregulated in patients with thymic hyperplasia accompanied by MG. Additionally, the abnormal activation of the thymic atrophy pathway may be one of the causes of autoreactive T cell production. This research provides a potential perspective on the pathogenesis of MG in patients with thymic hyperplasia.
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.