Enhanced expression of Fas ligand (CD95L) on T cells after segmental allergen provocation in asthma

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Abstract

Background: Little is known about the termination of the T-cell driven inflammation found in patients with allergic asthma. Objective: Because signals delivered through Fas/Fas ligand can lead to T-cell apoptosis, we investigated the expression of Fas and Fas ligand on peripheral blood- and bronchoalveolar lavage fluid (BALF)-derived T cells and the percentage of apoptotic BALF cells in asthma. Methods: Nine atopic subjects with mild asthma and 9 control subjects underwent segmental sham and allergen challenge. Flow cytometry was used to determine the T-cell expression of Fas and Fas ligand, and the terminal dUTP nick end labeled technique was applied to detect apoptotic BALF cells. Results: In asthmatic and control subjects almost all T cells in the BALF expressed Fas antigen without changes after saline or allergen challenge. A small percentage of T cells in BALF expressed the Fas ligand. In asthmatic subjects, but not in control subjects, there was a significant increase in Fas ligand after allergen challenge (CD3: 0.8% ± 0.6% [baseline] vs 3.2% ± 1.2% [allergen challenge]; CD4: 1.8% ± 0.0% vs 4.3% ± 1.8%; CD8: 2.8% ± 2.4% vs 9.1% ± 4.8%) but not after saline challenge, with a significant correlation to the percentage of BALF eosinophils. Apoptotic BALF cells were localized exclusively in macrophages at a very low frequency (0.03% to 0.15%) and without changes after saline or allergen challenge in both groups. Conclusion: In asthma there is an upregulation of Fas ligand on T cells in BALF after allergen challenge. Because there is no evidence for increased apoptosis, this phenomenon may reflect antigen-induced T-cell activation rather than apoptosis.

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Krug, N., Tschernig, T., Balke, K., Erpenbeck, V. J., Meyer, L., Bode, U., … Fabel, H. (1999). Enhanced expression of Fas ligand (CD95L) on T cells after segmental allergen provocation in asthma. Journal of Allergy and Clinical Immunology, 103(4), 649–655. https://doi.org/10.1016/S0091-6749(99)70238-1

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