The effects of anti-histone H1 antibody on immune cells responsible for rejection reaction.

نویسندگان

  • Li-Wen Hsu
  • Shigeru Goto
  • Toshiaki Nakano
  • Chia-Yun Lai
  • Ying-Hsien Kao
  • Yu-Chun Lin
  • Seiji Kawamoto
  • Kazuhisa Ono
  • Roger Lord
  • Takeshi Goto
  • Naoya Omori
  • Shuji Sato
  • Kuei-Chen Chiang
  • Shu-Hui Chen
  • Bruno Jawan
  • Yu-Fan Cheng
  • King-Wah Chiu
  • Chao-Long Chen
چکیده

We previously demonstrated the immunosuppressive activity of anti-histone H1 autoreactive antibodies (Ab) transiently induced in serum of a rat tolerogenic orthotopic liver transplantation (OLT) model. In the present study, we investigated the effects of anti-histone H1 Ab on dendritic cells (DCs), T-cells, lymphokine-activated killer (LAK) cells, and human natural killer (NK) cells. The effects of anti-histone H1 Ab on Concanavalin A (ConA) blast, on rat DC cytokine profiles and phenotypes, and on T-cells, LAK cells, and human NK cells were examined by flow cytometry and RT-PCR. The cytotoxicity of LAK and NK cells pretreated with anti-histone H1 Ab was assayed. The addition of anti-histone H1 Ab to ConA blast inhibited the proliferation of 5-(6)-carboxy-fluorescein succinimidyl ester (CFSE)-labeled lymphocytes without toxicity but increased the population of CD4+CD25+ T-cells. DCs treated with anti-histone H1 Ab expressed lower levels of CD80/CD86, IL-1beta, and IL-6. The addition of anti-histone H1 Ab to LAK culture decreased the percentages of NKR-P1 populations and down-regulated levels of inducible nitric oxide synthase (iNOS), IL-2, and INF-gamma in RT-PCR. The cytotoxicity of LAK and NK cells was lower when pretreated with anti-histone H1 Ab than when pretreated with control IgG. We found that the blockade of histone H1 modulated DCs toward tolerogenic status, decreased the cytotoxicity of LAK and NK cells, and induced CD4+CD25+ T-cells. These results suggest that the use of anti-histone H1 Abs might be a useful strategy for the development of a form of immunosuppression.

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عنوان ژورنال:
  • Molecular immunology

دوره 42 10  شماره 

صفحات  -

تاریخ انتشار 2005