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CTLA-4 methylation regulates the pathogenesis of myasthenia gravis and the expression of related cytokines.

Abstract Myasthenia gravis (MG) is a progressive autoimmune disease that occurs as a result of the failure of neuromuscular transmission and is characterized by muscle weakness. There has been evidence on the correlations between the genetic predisposition of cytotoxic T lymphocyte and the antigen-4 (CTLA-4) and MG. Thus, the present study was conducted to study is designed to examine the effects of CTLA-4 methylation on the pathogenesis of MG and the expressions of related cytokines.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title medicine
Publication Year Start




PMID- 29718870
OWN - NLM
STAT- MEDLINE
DCOM- 20180508
LR  - 20180508
IS  - 1536-5964 (Electronic)
IS  - 0025-7974 (Linking)
VI  - 97
IP  - 18
DP  - 2018 May
TI  - CTLA-4 methylation regulates the pathogenesis of myasthenia gravis and the
      expression of related cytokines.
PG  - e0620
LID - 10.1097/MD.0000000000010620 [doi]
AB  - BACKGROUND: Myasthenia gravis (MG) is a progressive autoimmune disease that
      occurs as a result of the failure of neuromuscular transmission and is
      characterized by muscle weakness. There has been evidence on the correlations
      between the genetic predisposition of cytotoxic T lymphocyte and the antigen-4
      (CTLA-4) and MG. Thus, the present study was conducted to study is designed to
      examine the effects of CTLA-4 methylation on the pathogenesis of MG and the
      expressions of related cytokines. METHODS: The CTLA-4 methylation levels in
      peripheral blood were quantified in 103 samples collected from MG patients and 86
      samples from healthy individiuals. The expression of serum-related cytokines as
      well as the Treg cell ratio were examined so as to define the contributory role
      of CTLA-4 methylation in MG and to identify the interaction between CTLA-4
      methylation and related factors, the expressions of DNA methyltransferase
      (DNMT)l, DNMT3A and DNMT3B, CTLA-4, AchR-Ab, Titin-Ab, RyR-Ab, IL-2, IL-10,
      IFN-gamma, and TGF-beta, activity of P- acetylcholinesterase (AchE) and E-AchE.
      RESULTS: The results indicated that the incidence of CTLA-4 methylation was
      significantly higher in the control group when compared with the MG group, and
      CTLA-4 methylation was also found to be associated with the thymus status of MG
      patients. It was also observed from the experiment data that the expressions of
      DNMTl, DNMT3A, and DNMT3B, along with the expressions of AchR-Ab, Titin-Ab,
      RyR-Ab, IL-2, IL-10, IFN-gamma and TGF-beta, and the activity of P-AchE and
      E-AchE were all higher in the MG group than in the control group, with a
      reduction of CTLA-4 expression. Another key finding from this study revealed that
      methylation interference can lead to the suppression in the expression of
      AchR-Ab, the activity of E-AchE, the expression of IL-2, IL-10, IFN-gamma, and
      TGF-beta and the Treg cell ratio in lymphocytes. CONCLUSION: In conclusion, the
      results obtained from the present study highly indicated that CTLA-4 methylation 
      might play a role in facilitating the occurrence of MG and increasing the
      expressions of related cytokines through the upregulation of AchR-Ab and E-Ach.
FAU - Fang, Ti-Kun
AU  - Fang TK
AD  - Department of Emergency, Jining No.1 People's Hospital, Jining, Shandong
      Province, P.R. China.
FAU - Yan, Cheng-Jun
AU  - Yan CJ
FAU - Du, Juan
AU  - Du J
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Medicine (Baltimore)
JT  - Medicine
JID - 2985248R
RN  - 0 (CTLA-4 Antigen)
RN  - 0 (CTLA4 protein, human)
RN  - 0 (Cytokines)
RN  - EC 3.1.1.7 (Acetylcholinesterase)
SB  - AIM
SB  - IM
MH  - Acetylcholinesterase/blood
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Animals
MH  - CTLA-4 Antigen/*blood
MH  - Child
MH  - Cytokines/*blood
MH  - Disease Models, Animal
MH  - Female
MH  - Humans
MH  - Male
MH  - Methylation
MH  - Middle Aged
MH  - Myasthenia Gravis/*blood/pathology
MH  - Rats, Inbred Lew
MH  - T-Lymphocytes, Regulatory/metabolism
MH  - Up-Regulation
MH  - Young Adult
EDAT- 2018/05/03 06:00
MHDA- 2018/05/09 06:00
CRDT- 2018/05/03 06:00
PHST- 2018/05/03 06:00 [entrez]
PHST- 2018/05/03 06:00 [pubmed]
PHST- 2018/05/09 06:00 [medline]
AID - 10.1097/MD.0000000000010620 [doi]
AID - 00005792-201805040-00038 [pii]
PST - ppublish
SO  - Medicine (Baltimore). 2018 May;97(18):e0620. doi: 10.1097/MD.0000000000010620.