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Interleukin‐10 is localized to and released by human lung mast cells
Author(s) -
Ishizuka,
Okayama,
Kazuya Kobayashi,
Taketoshi Mori
Publication year - 1999
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1046/j.1365-2222.1999.00636.x
Subject(s) - immunoglobulin e , interleukin 33 , mast cell , cytokine , immunocytochemistry , tryptase , interleukin 5 , immunology , stem cell factor , biology , interleukin 9 , microbiology and biotechnology , degranulation , receptor , inflammation , antibody , interleukin , chemistry , endocrinology , stem cell , biochemistry , haematopoiesis
Background Mast cells control the local inflammation by producing many kinds of cytokines. Interleukin (IL)‐10 is one of the important cytokine that upregulate or downregulate inflammation. Objective The aim of this study is to ascertain whether IL‐10 is produced from human lung mast cells by cross‐linkage of high‐affinity Fcε receptors (FcεRI). Methods Mast cells were purified using affinity magnetic selection with mAb YB5.B8 (> 93% pure). Mast cells were precultured with human myeloma IgE (3 μg/mL) for 16 h and then washed, and stimulated with anti‐IgE in the presence or absence of recombinant human stem cell factor (rhSCF). We have studied the production of IL‐10 by using reverse transcription‐PCR, enzyme‐linked immunosorbent assay and immunocytochemistry. Results We found that human lung mast cells were immunocytochemically stained with anti‐IL‐10 mAb after IgE‐dependent stimulation. The activation of mast cells via FcεRI enhanced the intensity of the IL‐10 mRNA signal. Anti‐IgE (1 μg/mL) induced a median IL‐10 release of 301.7 (7.8–1532.4) pg/10 6 mast cells/24 h. In contrast, mast cells released only a small amount of IL‐10 in the absence of anti‐IgE. This difference was statistically significant (P = 0.02, n = 11). Conclusion Our findings indicate that human lung mast cells are capable of producing IL‐10 in response to IgE‐dependent stimulation.