Pathogenesis of Autoimmune Hepatitis-Cellular and Molecular Mechanisms.
Animals
Azathioprine
/ therapeutic use
DNA Methylation
/ drug effects
Epigenesis, Genetic
/ drug effects
Glucocorticoids
/ therapeutic use
Hepatitis, Autoimmune
/ drug therapy
Humans
Immunosuppressive Agents
/ therapeutic use
Liver
/ immunology
Prednisolone
/ therapeutic use
RNA, Untranslated
/ genetics
T-Lymphocytes
/ drug effects
T cells
autoantibodies
autoimmune hepatitis
autoimmunity
genetic trait
pathogenesis
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
17 Dec 2021
17 Dec 2021
Historique:
received:
07
11
2021
revised:
09
12
2021
accepted:
14
12
2021
entrez:
24
12
2021
pubmed:
25
12
2021
medline:
18
1
2022
Statut:
epublish
Résumé
Pediatric autoimmune liver disorders include autoimmune hepatitis (AIH), autoimmune sclerosing cholangitis (ASC), and de novo AIH after liver transplantation. AIH is an idiopathic disease characterized by immune-mediated hepatocyte injury associated with the destruction of liver cells, causing inflammation, liver failure, and fibrosis, typically associated with autoantibodies. The etiology of AIH is not entirely unraveled, but evidence supports an intricate interaction among genetic variants, environmental factors, and epigenetic modifications. The pathogenesis of AIH comprises the interaction between specific genetic traits and molecular mimicry for disease development, impaired immunoregulatory mechanisms, including CD4+ T cell population and Treg cells, alongside other contributory roles played by CD8+ cytotoxicity and autoantibody production by B cells. These findings delineate an intricate pathway that includes gene to gene and gene to environment interactions with various drugs, viral infections, and the complex microbiome. Epigenetics emphasizes gene expression through hereditary and reversible modifications of the chromatin architecture without interfering with the DNA sequence. These alterations comprise DNA methylation, histone transformations, and non-coding small (miRNA) and long (lncRNA) RNA transcriptions. The current first-line therapy comprises prednisolone plus azathioprine to induce clinical and biochemical remission. Further understanding of the cellular and molecular mechanisms encountered in AIH may depict their impact on clinical aspects, detect biomarkers, and guide toward novel, effective, and better-targeted therapies with fewer side effects.
Identifiants
pubmed: 34948375
pii: ijms222413578
doi: 10.3390/ijms222413578
pmc: PMC8703580
pii:
doi:
Substances chimiques
Glucocorticoids
0
Immunosuppressive Agents
0
RNA, Untranslated
0
Prednisolone
9PHQ9Y1OLM
Azathioprine
MRK240IY2L
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
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