Non-Coding RNAs in Myasthenia Gravis: From Immune Regulation to Personalized Medicine

Myasthenia gravis (MG) is an antibody-mediated autoimmune disorder characterized by altered neuromuscular transmission, which causes weakness and fatigability in the skeletal muscles. The etiology of MG is complex, being associated with multiple genetic and environmental factors. Over recent years,...

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Published inCells (Basel, Switzerland) Vol. 13; no. 18; p. 1550
Main Authors Iacomino, Nicola, Tarasco, Maria Cristina, Berni, Alessia, Ronchi, Jacopo, Mantegazza, Renato, Cavalcante, Paola, Foti, Maria
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 01.09.2024
MDPI
Subjects
Adaptive immunity
Animals
Antibodies
Antigens
Autoimmune diseases
Autoimmunity
Autoimmunity - genetics
B cells
Biomarkers
Cytokines
Development and progression
Diagnostic tests
Disease
DNA methylation
Environmental factors
Epigenesis, Genetic
Epigenetic inheritance
Epigenetics
Genes
Genetic aspects
Homeostasis
Humans
Hyperplasia
Immune response
Immune system
Immunity (Disease)
Immunoregulation
Inflammation
Innate immunity
Kinases
long non-coding RNAs
Lymphocytes
MicroRNA
MicroRNAs
MicroRNAs - genetics
MicroRNAs - metabolism
miRNA
Muscles
Myasthenia gravis
Myasthenia Gravis - genetics
Myasthenia Gravis - immunology
Myasthenia Gravis - pathology
Myasthenia Gravis - therapy
Neuromuscular junctions
Neurophysiology
Non-coding RNA
Pathogenesis
Phenotypes
Precision medicine
Precision Medicine - methods
Review
RNA, Long Noncoding - genetics
RNA, Untranslated - genetics
Skeletal muscle
Stem cells
Thymus
Thymus gland
Viral antibodies
microRNAs
myasthenia gravis
autoimmunity
long non-coding RNAs
Online AccessGet full text
ISSN2073-4409
2073-4409
DOI10.3390/cells13181550

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Abstract Myasthenia gravis (MG) is an antibody-mediated autoimmune disorder characterized by altered neuromuscular transmission, which causes weakness and fatigability in the skeletal muscles. The etiology of MG is complex, being associated with multiple genetic and environmental factors. Over recent years, progress has been made in understanding the immunological alterations implicated in the disease, but the exact pathogenesis still needs to be elucidated. A pathogenic interplay between innate immunity and autoimmunity contributes to the intra-thymic MG development. Epigenetic changes are critically involved in both innate and adaptive immune response regulation. They can act as (i) pathological factors besides genetic predisposition and (ii) co-factors contributing to disease phenotypes or patient-specific disease course/outcomes. This article reviews the role of non-coding RNAs (ncRNAs) as epigenetic factors implicated in MG. Particular attention is dedicated to microRNAs (miRNAs), whose expression is altered in MG patients’ thymuses and circulating blood. The long ncRNA (lncRNA) contribution to MG, although not fully characterized yet, is also discussed. By summarizing the most recent and fast-growing findings on ncRNAs in MG, we highlight the therapeutic potential of these molecules for achieving immune regulation and their value as biomarkers for the development of personalized medicine approaches to improve disease care.
AbstractList Myasthenia gravis (MG) is an antibody-mediated autoimmune disorder characterized by altered neuromuscular transmission, which causes weakness and fatigability in the skeletal muscles. The etiology of MG is complex, being associated with multiple genetic and environmental factors. Over recent years, progress has been made in understanding the immunological alterations implicated in the disease, but the exact pathogenesis still needs to be elucidated. A pathogenic interplay between innate immunity and autoimmunity contributes to the intra-thymic MG development. Epigenetic changes are critically involved in both innate and adaptive immune response regulation. They can act as (i) pathological factors besides genetic predisposition and (ii) co-factors contributing to disease phenotypes or patient-specific disease course/outcomes. This article reviews the role of non-coding RNAs (ncRNAs) as epigenetic factors implicated in MG. Particular attention is dedicated to microRNAs (miRNAs), whose expression is altered in MG patients' thymuses and circulating blood. The long ncRNA (lncRNA) contribution to MG, although not fully characterized yet, is also discussed. By summarizing the most recent and fast-growing findings on ncRNAs in MG, we highlight the therapeutic potential of these molecules for achieving immune regulation and their value as biomarkers for the development of personalized medicine approaches to improve disease care.Myasthenia gravis (MG) is an antibody-mediated autoimmune disorder characterized by altered neuromuscular transmission, which causes weakness and fatigability in the skeletal muscles. The etiology of MG is complex, being associated with multiple genetic and environmental factors. Over recent years, progress has been made in understanding the immunological alterations implicated in the disease, but the exact pathogenesis still needs to be elucidated. A pathogenic interplay between innate immunity and autoimmunity contributes to the intra-thymic MG development. Epigenetic changes are critically involved in both innate and adaptive immune response regulation. They can act as (i) pathological factors besides genetic predisposition and (ii) co-factors contributing to disease phenotypes or patient-specific disease course/outcomes. This article reviews the role of non-coding RNAs (ncRNAs) as epigenetic factors implicated in MG. Particular attention is dedicated to microRNAs (miRNAs), whose expression is altered in MG patients' thymuses and circulating blood. The long ncRNA (lncRNA) contribution to MG, although not fully characterized yet, is also discussed. By summarizing the most recent and fast-growing findings on ncRNAs in MG, we highlight the therapeutic potential of these molecules for achieving immune regulation and their value as biomarkers for the development of personalized medicine approaches to improve disease care.
Myasthenia gravis (MG) is an antibody-mediated autoimmune disorder characterized by altered neuromuscular transmission, which causes weakness and fatigability in the skeletal muscles. The etiology of MG is complex, being associated with multiple genetic and environmental factors. Over recent years, progress has been made in understanding the immunological alterations implicated in the disease, but the exact pathogenesis still needs to be elucidated. A pathogenic interplay between innate immunity and autoimmunity contributes to the intra-thymic MG development. Epigenetic changes are critically involved in both innate and adaptive immune response regulation. They can act as (i) pathological factors besides genetic predisposition and (ii) co-factors contributing to disease phenotypes or patient-specific disease course/outcomes. This article reviews the role of non-coding RNAs (ncRNAs) as epigenetic factors implicated in MG. Particular attention is dedicated to microRNAs (miRNAs), whose expression is altered in MG patients’ thymuses and circulating blood. The long ncRNA (lncRNA) contribution to MG, although not fully characterized yet, is also discussed. By summarizing the most recent and fast-growing findings on ncRNAs in MG, we highlight the therapeutic potential of these molecules for achieving immune regulation and their value as biomarkers for the development of personalized medicine approaches to improve disease care.
Audience Academic
Author Cavalcante, Paola
Foti, Maria
Mantegazza, Renato
Iacomino, Nicola
Ronchi, Jacopo
Berni, Alessia
Tarasco, Maria Cristina
AuthorAffiliation 2 Ph.D. Program in Neuroscience, University of Milano-Bicocca, 20900 Monza, Italy; jacopo.ronchi@unimib.it
4 BicOMICs, University of Milano-Bicocca, 20900 Monza, Italy
1 Neurology 4–Neuroimmunology and Neuromuscolar Diseases, Fondazione IRCCS Istituto Neurologico Carlo Besta, 20133 Milan, Italy; nicola.iacomino@istituto-besta.it (N.I.); mariacristina.tarasco@istituto-besta.it (M.C.T.); alessia.berni@istituto-besta.it (A.B.); renato.mantegazza@istituto-besta.it (R.M.)
3 Department of Medicine and Surgery, University of Milano-Bicocca, 20900 Monza, Italy
AuthorAffiliation_xml – name: 1 Neurology 4–Neuroimmunology and Neuromuscolar Diseases, Fondazione IRCCS Istituto Neurologico Carlo Besta, 20133 Milan, Italy; nicola.iacomino@istituto-besta.it (N.I.); mariacristina.tarasco@istituto-besta.it (M.C.T.); alessia.berni@istituto-besta.it (A.B.); renato.mantegazza@istituto-besta.it (R.M.)
– name: 2 Ph.D. Program in Neuroscience, University of Milano-Bicocca, 20900 Monza, Italy; jacopo.ronchi@unimib.it
– name: 3 Department of Medicine and Surgery, University of Milano-Bicocca, 20900 Monza, Italy
– name: 4 BicOMICs, University of Milano-Bicocca, 20900 Monza, Italy
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CitedBy_id crossref_primary_10_3389_fimmu_2025_1549034
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Keywords microRNAs
myasthenia gravis
autoimmunity
long non-coding RNAs
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Snippet Myasthenia gravis (MG) is an antibody-mediated autoimmune disorder characterized by altered neuromuscular transmission, which causes weakness and fatigability...
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SubjectTerms Adaptive immunity
Animals
Antibodies
Antigens
Autoimmune diseases
Autoimmunity
Autoimmunity - genetics
B cells
Biomarkers
Cytokines
Development and progression
Diagnostic tests
Disease
DNA methylation
Environmental factors
Epigenesis, Genetic
Epigenetic inheritance
Epigenetics
Genes
Genetic aspects
Homeostasis
Humans
Hyperplasia
Immune response
Immune system
Immunity (Disease)
Immunoregulation
Inflammation
Innate immunity
Kinases
long non-coding RNAs
Lymphocytes
MicroRNA
MicroRNAs
MicroRNAs - genetics
MicroRNAs - metabolism
miRNA
Muscles
Myasthenia gravis
Myasthenia Gravis - genetics
Myasthenia Gravis - immunology
Myasthenia Gravis - pathology
Myasthenia Gravis - therapy
Neuromuscular junctions
Neurophysiology
Non-coding RNA
Pathogenesis
Phenotypes
Precision medicine
Precision Medicine - methods
Review
RNA, Long Noncoding - genetics
RNA, Untranslated - genetics
Skeletal muscle
Stem cells
Thymus
Thymus gland
Viral antibodies
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Title Non-Coding RNAs in Myasthenia Gravis: From Immune Regulation to Personalized Medicine
URI https://www.ncbi.nlm.nih.gov/pubmed/39329732
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Volume 13
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