Activation-induced cell death of peripheral blood T lymphocytes in patients with primary Sjögren’s syndrome

summaryIFNg plays an important role to induce several functional molecules on salivary epithelial cells, including class II MHC, Fas and CD40 in salivary glands from patients with Sj äogren's syndrome (SS). IFNg also contributes to the development of lymphocytic inˆltrates by inducing T cell attracting chemokines in SS salivary epithelial cells, such as IP 10（CXCL10), Mig（CXCL9), and I TAC (CXCL11). IFNg dysregulation in SS salivary gland may attribute to the decreased production of TGFb from salivary epithelial cells in some patients. Expression of Fas and CD40 was signiˆcantly higher in SS salivary epithelial cells than in normal cells after IFNg stimulation. Although neither anti Fas (CH11) nor anti CD40 mAb alone could induce typical apoptosis, the two together and preincubation with IFNg e‹ciently induced apoptosis in SS salivary epithelial cells. This apoptosis was almost completely blocked by neutralizing anti Fas mAb (ZB4). c FLIP, an important inhibitory molecule in the Fas death pathway, was strongly expressed in SS salivary epithelial cells, but its expression was downregulated, at the protein level, by anti CD40 mAb. CD40 signals promote Fas dependent death of SS salivary epithelial cells by downregulating c FLIP expression. The presence of c FLIP in these cells may explain their resistance to undergo apoptosis in response to either anti Fas or anti CD40 mAb, despite their surface expression of both proteins. Theseˆndings suggest that SS salivary epithelial cell death requires the cooperation of Fas and CD40.

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シェーグレン症候群における唾液腺組織障害の分子機構

Ogawa

Shimoyama

Kawanami

2005

Jpn. J. Clin. Immunol.

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Activation-induced cell death of peripheral blood T lymphocytes in patients with primary Sjögren’s syndrome

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References 23 publications

シェーグレン症候群における唾液腺組織障害の分子機構

シェーグレン症候群における唾液腺組織障害の分子機構

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