タナカ, ハルコ Third Department of Internal Medicine, The University of Tokushima School of Medicine
ナカムラ, ヨウイチ Third Department of Internal Medicine, The University of Tokushima School of Medicine
吾妻, 雅彦 Third Department of Internal Medicine, The University of Tokushima School of Medicine 徳島大学 教育研究者総覧 KAKEN研究者をさがす
楊河, 宏章 Third Department of Internal Medicine, The University of Tokushima School of Medicine 徳島大学 教育研究者総覧 KAKEN研究者をさがす
bronchial epithelial cells
We examined whether freshly isolated human bronchial cells (HBEC) and bronchial epithelial cell line/ BEAS-2B cells expressed surface molecules required for APC function. These cells expressed CD40 and ICAM-1, but not B7-1, B7-2 or HLA-DR molecules. Treatment of these cells with IFN-γ resulted in enhanced expression of CD40 and ICAM-1 as well as induction of HLA-DR expression. Th2 cytokines such as IL-4 and IL-5, proinflammatory cytokine of GM-CSF and nonspecific activator endotoxin had no effect on these phenotypic expressions. Functional examinations showed that allogeneic lymphocytes purified from peripheral blood strongly proliferated in response to BEAS-2B cells cultured with IFN-γ, but only weakly compared with those without IFN-γ. When allogeneic lymphocytes were purified to CD4+ cells, the proliferative response against BEAS-2B cells was abolished. Blockade of CD40-CD40L interaction by anti-CD40 antibody also inhibited the proliferation of lymphocytes to BEAS-2B cells, although this treatment showed a minimum effect on the response to allogeneic MNC. Thus, bronchial epithelial cells have the ability to present allogeneic antigens to T cells in both CD40- and IFN-γ- dependent manners under the presence of third party cells that transduce co-stimulatory signals.
The journal of medical investigation : JMI
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