The mechanisms responsible for thyrocyte destruction in Hashimoto's thyroiditis (HT) are poorly understood. Thyrocytes from HT glands, but not from nonautoimmune thyroids, expressed Fas. Interleukin-1beta (IL-1beta), abundantly produced in HT glands, induced Fas expression in normal thyrocytes, and cross-linking of Fas resulted in massive thyrocyte apoptosis. The ligand for Fas (FasL) was shown to be constitutively expressed both in normal and HT thyrocytes and was able to kill Fas-sensitive targets. Exposure to IL-1beta induced thyrocyte apoptosis, which was prevented by antibodies that block Fas, suggesting that IL-1beta-induced Fas expression serves as a limiting factor for thyrocyte destruction. Thus, Fas-FasL interactions among HT thyrocytes may contribute to clinical hypothyroidism.

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Intercellular adhesion molecule 1 (ICAM-1 or CD54) expression on epithelial cells (EC) has been demonstrated to play a role in the local molecular events of inflammation following allergen-specific conjunctival challenge. In the light of these observations, we evaluated the possible expression of ICAM-1 on nasal EC after allergen-specific challenge. Three groups of subjects were studied: (1) 14 symptomless patients sensitized to mites, (2) 15 symptomless patients sensitized to pollen, and (3) 10 healthy volunteers as controls. The study was performed during winter. At baseline we found that both pollinosic and healthy subjects did not express CD54 on epithelial cells, whereas mite-sensitive patients showed a mild expression (possibly caused by a persistent natural allergen exposure). In addition, clinical and cellular responses were induced by lower allergen dosages in mite-sensitive patients compared with pollen-sensitive patients. CD54 was detectable in all the allergic patients but not in the control subjects 30 min after challenge. At 6 h all patients showed a marked inflammatory infiltration and CD54 persistence on EC: such an infiltration was more relevant in patients developing clinical late-phase reaction (LPR). Finally, 24 h after challenge EC CD54 expression persisted, as well as a cellular infiltrate mainly caused by eosinophils (the latter being more pronounced in mite-sensitive individuals). CD54 should be regarded as an early and sensitive marker of inflammation in both LPR-positive and LPR-negative patients. A cellular inflammatory infiltrate was detectable in both LPR-positive and LPR-negative subjects, although relevant differences in eosinophil counts were observed between the two groups. The study emphasizes the importance of the different events of inflammation in allergy.

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