2018, Number 6
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Ann Hepatol 2018; 17 (6)
Association of Interleukin-6 and Interleukin-1 Family Gene Polymorphisms in Autoimmune Hepatitis
Yousefi A, Najafi M, Motamed F, Mahmoudi E, Zare BA, Sadr M, Rahmani F, Farhmand F, Khodadad A, Fallahi G, Rezaei N
Language: English
References: 37
Page: 1021-1025
PDF size: 138.75 Kb.
ABSTRACT
Introduction and aim. Autoimmune hepatitis (AIH) is an immune-mediated destruction of liver cells, in recognition of interface
hepatitis, seropositivity for autoantibodies, and interface hepatitis in histology sections. Hepatocyte destruction in AIH is the direct
result of CD4+ T-cell destruction. Yet, Th17 mediated immune attach and a diversity of cytokine networks, including pro-inflammatory
cytokines such as Interleukin 1 (IL-1) and Interleukin 6 (IL-6), set the stage for the destructive liver damage.
Material and
method. Peripheral blood samples from 57 patients, with AIH, recruited from referrals to the main pediatric hospital in Tehran. Single
nucleotide polymorphisms for the following cytokines genes, were evaluated through, polymerase chain reaction with sequencespecific
primers (PCR-SSP) assay: IL-1a (C/T -889), IL-1α (C/T -511), IL-1β (C/T +3962), IL-1 receptor (IL-1R; C/T Pst-I 1970),
IL-1RA (C/T Mspa-I 11100), and IL-6 (C/G -174 and A/G nt565).
Results. Significant higher frequency of genotype AA was detected
in patients in IL-6 at position nt565 (15.8% in AIH patients
vs. 2.9% in controls, p = 0.003). The haplotype GA of IL-6 at -174
and nt565, was significantly overrepresented in the AIH group, compared to (20.9% of AIH vs. 1.4% in controls p ‹ 0.0001).
Conclusion.
Results of our study, indicate significant deviation toward high yield IL-6 polymorphisms, in AIH patients. These data could
bring new insights in pathophysiology of disease, which could contribute to developing novel treatments for AIH.
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