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Regulation of tumour necrosis factor‐related apoptosis‐inducing ligand (TRAIL) and TRAIL receptor expression in human neutrophils
Author(s) -
Kamohara Hidenobu,
Matsuyama Wataru,
Shimozato Osamu,
Abe Koichiro,
Galligan Carole,
Hashimoto ShinIchi,
Matsushima Kouji,
Yoshimura Teizo
Publication year - 2004
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.0019-2805.2003.01794.x
Subject(s) - tumor necrosis factor alpha , apoptosis , receptor , biology , microbiology and biotechnology , necrosis , cytokine , immunology , immune system , cell , receptor expression , cell culture , genetics
Summary Tumour necrosis factor (TNF)‐related apoptosis‐inducing ligand (TRAIL) is a member of the TNF superfamily, which is capable of inducing apoptosis in many cell types, including tumour and virus‐infected cells, but rarely in normal cells. Expression of TRAIL mRNA and TRAIL receptors has previously been detected in neutrophils; however, the expression of TRAIL protein and the regulation of TRAIL and TRAIL receptor expression in these cells remain unknown. Here we report, for the first time, that neutrophils constitutively express TRAIL protein on their cell surface and that the TRAIL protein is shed during culture. TNF‐α is a down‐regulator of TRAIL expression, whereas IFN‐γ up‐regulates the expression of TRAIL. Neutrophils did not express a detectable level of TRAIL‐R1 or ‐R4, but constitutively expressed a low, but substantial, level of TRAIL‐R2 and a high level of TRAIL‐R3. Although the level of TRAIL‐R2 was not significantly altered during culture under different experimental conditions, ≈ 30% of TNF‐α‐treated cells rapidly lost their high‐level TRAIL‐R3 expression, whereas the majority of IFN‐γ‐treated cells retained a high level of TRAIL‐R3 expression. Anti‐TRAIL neutralizing antibody significantly inhibited neutrophil apoptosis during cultures in medium alone, or in the presence of TNF‐α or IFN‐γ. Thus, our study identified human neutrophils as a cellular source of TRAIL and suggests that neutrophil‐derived TRAIL may play a role in immune surveillance. Our results also suggest a role for the TRAIL/TRAIL receptor system in neutrophil apoptosis.