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Interleukin‐27 as a Negative Regulator of Human Neutrophil Function
Author(s) -
Li J. P.,
Wu H.,
Xing W.,
Yang S. G.,
Lu S. H.,
Du W. T.,
Yu J. X.,
Chen F.,
Zhang L.,
Han Z. C.
Publication year - 2010
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2010.02422.x
Subject(s) - immune system , microbiology and biotechnology , major histocompatibility complex , immunology , biology , innate immune system , cytotoxic t cell , cytokine , tumor necrosis factor alpha , interleukin , lipopolysaccharide , chemistry , in vitro , biochemistry
Interleukin‐27 (IL‐27) is a novel cytokine of the IL‐6/12 family with a broad range of immune regulation properties, which has been considered as a potential therapeutic agent for immune diseases and cancers. However, little is known about the effect of IL‐27 on human neutrophils before its clinical administration. In this study, we investigated the effects of IL‐27 on human neutrophil functions including adhesion, reactive oxygen species (ROS)/cytotoxic granule components production, inflammatory cytokines production, major histocompatibility complex (MHC) molecules expression and neutrophils’ survival. We showed that IL‐27 receptor complex, WSX‐1/TCCR and gp130, is constitutively expressed on human neutrophils. In vitro , IL‐27 suppressed neutrophil adhesion in response to fMLP, which might depend on the down‐regulation of Mac‐1. IL‐27 also suppressed lipopolysaccharide‐induced ROS production and attenuated cytotoxic granule components production in the cytoplasm of human neutrophils. In addition, IL‐27 enhanced the production of IL‐1β but not TNF‐α from neutrophils. However, IL‐27 failed to regulate the expression of MHC molecules and the survival of human neutrophils. In conclusion, our data demonstrate that IL‐27 mainly down‐modulates human neutrophil function, which might extend our understanding of the role of IL‐27 in the innate immune response.