The detection of IRF-1 promoter polymorphisms and their possible contribution to T helper 1 response in chronic hepatitis C

Hidetsugu Saito, Shinichiro Tada, Kanji Wakabayashi, Nobuhiro Nakamoto, Masahiko Takahashi, Mitsuyasu Nakamura, Hirotoshi Ebinuma, Hiromasa Ishii

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

We described the interferon (IFN) regulatory factor-1 (IRF-1) promoter single nucleotide polymorphisms (SNPs), and the clinical and immunologic implications of these SNPs have been investigated. We successfully determined the mutation at -300 of the IRF-1 promoter by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), and this mutation linked with other mutations in the promoter region. In our Japanese population, the frequency of the type -300*A/A was 11.9%, type A/G was 54.2%, and type G/G was 33.9%. We found no significant difference without IFN stimulation in the production levels of IFN-γ and interleukin-10 (IL-10) from peripheral blood mononuclear cells (PBMC) between subjects with -300*A/A and those with other types. IFN-α stimulation, however, increased the levels of IFN-γ significantly and decreased the IL-10 production level significantly only in the subject with -300*A/A type. Flow cytometric analysis showed that the Th1-type CD4+ cell population was significantly increased by IFN-β administration only in the patient with chronic hepatitis C with -300*A/A type. These results suggest that the IRF-1 promoter SNP types are positively involved in Th1-type response and, consequently, the -300*A/A type may be beneficial for viral elimination in chronic hepatitis C and IFN therapy.

Original languageEnglish
Pages (from-to)693-700
Number of pages8
JournalJournal of Interferon and Cytokine Research
Volume22
Issue number6
DOIs
Publication statusPublished - 2002

Fingerprint

Chronic Hepatitis C
Interferons
Single Nucleotide Polymorphism
Interleukin-10
Mutation
Interferon Regulatory Factor-1
Th1 Cells
Genetic Promoter Regions
Restriction Fragment Length Polymorphisms
Population
Blood Cells
Polymerase Chain Reaction

ASJC Scopus subject areas

  • Immunology
  • Virology
  • Cell Biology

Cite this

The detection of IRF-1 promoter polymorphisms and their possible contribution to T helper 1 response in chronic hepatitis C. / Saito, Hidetsugu; Tada, Shinichiro; Wakabayashi, Kanji; Nakamoto, Nobuhiro; Takahashi, Masahiko; Nakamura, Mitsuyasu; Ebinuma, Hirotoshi; Ishii, Hiromasa.

In: Journal of Interferon and Cytokine Research, Vol. 22, No. 6, 2002, p. 693-700.

Research output: Contribution to journalArticle

Saito, Hidetsugu ; Tada, Shinichiro ; Wakabayashi, Kanji ; Nakamoto, Nobuhiro ; Takahashi, Masahiko ; Nakamura, Mitsuyasu ; Ebinuma, Hirotoshi ; Ishii, Hiromasa. / The detection of IRF-1 promoter polymorphisms and their possible contribution to T helper 1 response in chronic hepatitis C. In: Journal of Interferon and Cytokine Research. 2002 ; Vol. 22, No. 6. pp. 693-700.
@article{57513a45c38d46809d1073fcbee08067,
title = "The detection of IRF-1 promoter polymorphisms and their possible contribution to T helper 1 response in chronic hepatitis C",
abstract = "We described the interferon (IFN) regulatory factor-1 (IRF-1) promoter single nucleotide polymorphisms (SNPs), and the clinical and immunologic implications of these SNPs have been investigated. We successfully determined the mutation at -300 of the IRF-1 promoter by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), and this mutation linked with other mutations in the promoter region. In our Japanese population, the frequency of the type -300*A/A was 11.9{\%}, type A/G was 54.2{\%}, and type G/G was 33.9{\%}. We found no significant difference without IFN stimulation in the production levels of IFN-γ and interleukin-10 (IL-10) from peripheral blood mononuclear cells (PBMC) between subjects with -300*A/A and those with other types. IFN-α stimulation, however, increased the levels of IFN-γ significantly and decreased the IL-10 production level significantly only in the subject with -300*A/A type. Flow cytometric analysis showed that the Th1-type CD4+ cell population was significantly increased by IFN-β administration only in the patient with chronic hepatitis C with -300*A/A type. These results suggest that the IRF-1 promoter SNP types are positively involved in Th1-type response and, consequently, the -300*A/A type may be beneficial for viral elimination in chronic hepatitis C and IFN therapy.",
author = "Hidetsugu Saito and Shinichiro Tada and Kanji Wakabayashi and Nobuhiro Nakamoto and Masahiko Takahashi and Mitsuyasu Nakamura and Hirotoshi Ebinuma and Hiromasa Ishii",
year = "2002",
doi = "10.1089/10799900260100196",
language = "English",
volume = "22",
pages = "693--700",
journal = "Journal of Interferon and Cytokine Research",
issn = "1079-9907",
publisher = "Mary Ann Liebert Inc.",
number = "6",

}

TY - JOUR

T1 - The detection of IRF-1 promoter polymorphisms and their possible contribution to T helper 1 response in chronic hepatitis C

AU - Saito, Hidetsugu

AU - Tada, Shinichiro

AU - Wakabayashi, Kanji

AU - Nakamoto, Nobuhiro

AU - Takahashi, Masahiko

AU - Nakamura, Mitsuyasu

AU - Ebinuma, Hirotoshi

AU - Ishii, Hiromasa

PY - 2002

Y1 - 2002

N2 - We described the interferon (IFN) regulatory factor-1 (IRF-1) promoter single nucleotide polymorphisms (SNPs), and the clinical and immunologic implications of these SNPs have been investigated. We successfully determined the mutation at -300 of the IRF-1 promoter by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), and this mutation linked with other mutations in the promoter region. In our Japanese population, the frequency of the type -300*A/A was 11.9%, type A/G was 54.2%, and type G/G was 33.9%. We found no significant difference without IFN stimulation in the production levels of IFN-γ and interleukin-10 (IL-10) from peripheral blood mononuclear cells (PBMC) between subjects with -300*A/A and those with other types. IFN-α stimulation, however, increased the levels of IFN-γ significantly and decreased the IL-10 production level significantly only in the subject with -300*A/A type. Flow cytometric analysis showed that the Th1-type CD4+ cell population was significantly increased by IFN-β administration only in the patient with chronic hepatitis C with -300*A/A type. These results suggest that the IRF-1 promoter SNP types are positively involved in Th1-type response and, consequently, the -300*A/A type may be beneficial for viral elimination in chronic hepatitis C and IFN therapy.

AB - We described the interferon (IFN) regulatory factor-1 (IRF-1) promoter single nucleotide polymorphisms (SNPs), and the clinical and immunologic implications of these SNPs have been investigated. We successfully determined the mutation at -300 of the IRF-1 promoter by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), and this mutation linked with other mutations in the promoter region. In our Japanese population, the frequency of the type -300*A/A was 11.9%, type A/G was 54.2%, and type G/G was 33.9%. We found no significant difference without IFN stimulation in the production levels of IFN-γ and interleukin-10 (IL-10) from peripheral blood mononuclear cells (PBMC) between subjects with -300*A/A and those with other types. IFN-α stimulation, however, increased the levels of IFN-γ significantly and decreased the IL-10 production level significantly only in the subject with -300*A/A type. Flow cytometric analysis showed that the Th1-type CD4+ cell population was significantly increased by IFN-β administration only in the patient with chronic hepatitis C with -300*A/A type. These results suggest that the IRF-1 promoter SNP types are positively involved in Th1-type response and, consequently, the -300*A/A type may be beneficial for viral elimination in chronic hepatitis C and IFN therapy.

UR - http://www.scopus.com/inward/record.url?scp=0036376634&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036376634&partnerID=8YFLogxK

U2 - 10.1089/10799900260100196

DO - 10.1089/10799900260100196

M3 - Article

C2 - 12162881

AN - SCOPUS:0036376634

VL - 22

SP - 693

EP - 700

JO - Journal of Interferon and Cytokine Research

JF - Journal of Interferon and Cytokine Research

SN - 1079-9907

IS - 6

ER -