Negative Regulation of NK Cell Activities by Inhibitory Receptor CD94/NKG2A Leads to Altered NK Cell-Induced Modulation of Dendritic Cell Functions in Chronic Hepatitis C Virus Infection

DOI PDF PubMed 被引用文献8件 オープンアクセス
  • Masahisa Jinushi
    Department of Molecular Therapeutics, Osaka University Graduate School of Medicine , Osaka ,
  • Tetsuo Takehara
    Department of Molecular Therapeutics, Osaka University Graduate School of Medicine , Osaka ,
  • Tomohide Tatsumi
    Department of Molecular Therapeutics, Osaka University Graduate School of Medicine , Osaka ,
  • Tatsuya Kanto
    Department of Molecular Therapeutics, Osaka University Graduate School of Medicine , Osaka ,
  • Takuya Miyagi
    Department of Molecular Therapeutics, Osaka University Graduate School of Medicine , Osaka ,
  • Takahiro Suzuki
    Department of Molecular Therapeutics, Osaka University Graduate School of Medicine , Osaka ,
  • Yoshiyuki Kanazawa
    Department of Molecular Therapeutics, Osaka University Graduate School of Medicine , Osaka ,
  • Naoki Hiramatsu
    Department of Molecular Therapeutics, Osaka University Graduate School of Medicine , Osaka ,
  • Norio Hayashi
    Department of Molecular Therapeutics, Osaka University Graduate School of Medicine , Osaka ,

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公開日
2004-11
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.4049/jimmunol.173.10.6072
公開者
Oxford University Press (OUP)

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<jats:title>Abstract</jats:title> <jats:p>NK cells are potent activators of dendritic cells (DCs), but it remains obscure how third-party cells affect the ability of NK cells to modulate DC functions. We show here that NK cells derived from healthy donors (N-NK), when cocultured with human liver epithelial cells, induced maturation as well as activation of DCs, such as increased migratory capacity as well as T cell stimulatory activity. In contrast, NK cells from chronic hepatitis C virus-infected donors (HCV-NK) were not capable of activating DCs under the same conditions. In comparison to N-NK, HCV-NK showed higher expression of CD94/NKG2A and produced IL-10 and TGFβ when cultured with hepatic cells, most of which express HLA-E, a ligand for CD94/NKG2A. Blockade of NKG2A restored the ability of HCV-NK to activate DCs, which appeared to result from the reduced NK cell production of IL-10 and TGFβ. The blockade also endowed HCV-NK with an ability to drive DCs to generate Th1-polarized CD4+ T cells. These findings show that NK cell modulation of DCs is regulated by third-party cells through NK receptor and its ligand interaction. Aberrant expression of NK receptors may have an impact on the magnitude and direction of DC activation of T cells under pathological conditions, such as chronic viral infection.</jats:p>

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