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Cytokine induction of interleukin‐24 in human peripheral blood mononuclear cells
Author(s) -
Poindexter Nancy J.,
Walch Eugene T.,
Chada Sunil,
Grimm Elizabeth A.
Publication year - 2005
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0205116
Subject(s) - biology , peripheral blood mononuclear cell , cytokine , tumor necrosis factor alpha , microbiology and biotechnology , interleukin 19 , immunology , interleukin , interleukin 5 , in vitro , biochemistry
Interleukin‐24 (IL‐24) is a recently identified member of the IL‐10 family of cytokines. It was originally identified as a tumor suppressor molecule, melanoma differentiation‐associated gene 7, and then renamed IL‐24 and classified as a cytokine, based on its chromosomal location in the IL‐10 locus, its mRNA expression in leukocytes, and its secretory sequence elements. Here, we correlate the kinetics of IL‐24 mRNA and protein expression in human peripheral blood mononuclear cells (PBMC) stimulated by polyclonal activators phytohemagglutinin (PHA) and lipopolysaccharide (LPS) or by allogeneic major histocompatbility complex. PHA‐stimulated PBMC express IL‐24 mRNA, reaching peak levels at 8–12 h after stimulation. Protein expression, as measured by intracellular flow cytometry, followed the message, reaching maximum expression at 24 h. Subset analysis of mitogen‐stimulated PBMC showed that IL‐24 was expressed primarily in T cells and macrophages. Expression of IL‐24 in mitogen‐stimulated PBMC is the result of cytokine stimulation. Individual cytokines including IL‐2, IL‐7, IL‐15, tumor necrosis factor α, granulocyte macrophage‐colony stimulating factor, and IL‐1β stimulate the expression of IL‐24 mRNA and protein, whereas interferons and T helper cell type 2 cytokines fail to induce substantial IL‐24. When LPS‐ or PHA‐stimulated cells were treated with Actinomycin D, IL‐24 mRNA persisted at high levels over the 4‐h course of treatment. These data strongly suggest that the expression of IL‐24 in human PBMC results from cytokine stimulation and is regulated at the post‐transcriptional level through stabilization of IL‐24 mRNA.