Interleukin 10: a novel stimulatory factor for mast cells and their progenitors.

Thompson-Snipes, LuAnn; Dhar, Vineeta; Bond, Michael D.; Mosmann, Tim R.; Moore, Kevin W.; Rennick, Donna

doi:10.1084/jem.173.2.507

Cited by 486 publications

(214 citation statements)

References 13 publications

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“…Several new members of the IL-10 family, including IL-19, IL-20, IL-22, melanoma differentiation-associated gene (MDA) [3][4][5][6][7], and AK155 (IL-26), have only recently been discovered. The IL-19, IL-20, and MDA-7 (IL-24) genes have been mapped on chromosome 1q31-32, a region where IL-10 is located.…”

Section: Il-19 Induces Production Of Il-6 and Tnf-␣ And Results Inmentioning

confidence: 99%

IL-19 Induces Production of IL-6 and TNF-α and Results in Cell Apoptosis Through TNF-α

Liao

Liang

Chen

et al. 2002

The Journal of Immunology

308

235

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IL-10 is an immunosuppressive cytokine in the immune system. It was in clinical trail as an anti-inflammatory therapy for inflammatory bowel disease and various autoimmune diseases such as psoriasis, rheumatoid arthritis, and multiple sclerosis. IL-19 belongs to the IL-10 family, which includes IL-10, IL-19, IL-20, IL-22, melanoma differentiation-associated gene (MDA-7, IL-24), and AK155 (IL-26). Despite a partial homology in their amino acid sequences, they are dissimilar in their biologic functions. Little is known about the biologic function and gene regulation of IL-19. To understand the gene regulation of human IL-19, we identified a human IL-19 genomic clone and analyzed its promoter region. Five fusion genes containing different regions upstream of exon 1 linked to a luciferase reporter gene were expressed in the canine kidney epithelial-like Madin-Darby canine kidney cells. A fusion gene containing 394 bp showed luciferase activity 7- to 8-fold higher than the negative control of the promoterless fusion gene. We also isolated a full-length mouse cDNA clone. Mouse IL-19 shared 71% amino acid identity with human IL-19. Treatment of monocytes with mouse IL-19 induced the production of IL-6 and TNF-α. It also induced mouse monocyte apoptosis and the production of reactive oxygen species. Taken together, our results indicate that mouse IL-19 may play some important roles in inflammatory responses because it up-regulates IL-6 and TNF-α and induces apoptosis.

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Section: Il-19 Induces Production Of Il-6 and Tnf-␣ And Results Inmentioning

confidence: 99%

IL-19 Induces Production of IL-6 and TNF-α and Results in Cell Apoptosis Through TNF-α

Liao

Liang

Chen

et al. 2002

The Journal of Immunology

308

235

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“…17 and 18). IL-10 has been shown to regulate mast cell function, proliferation, survival, development, and protease gene expression (23)(24)(25)(26). Our observation that IL-10 mimicked the IL-4-mediated inhibition of mast cell Kit expression (15), combined with IL-4 plus IL-10-induced mast cell apoptosis (28) made Fc⑀RI studies logical.…”

Section: Discussionmentioning

confidence: 99%

IL-10 Inhibits FcεRI Expression in Mouse Mast Cells

Gillespie

DeMartino

Zhu

et al. 2004

The Journal of Immunology

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FcεRI expression and function is a central aspect of allergic disease. Using bone marrow-derived mouse mast cell populations, we have previously shown that the Th2 cytokine IL-4 inhibits FcεRI expression and function. In the current study we show that the Th2 cytokine IL-10 has similar regulatory properties, and that it augments the inhibitory effects of IL-4. FcεRI down-regulation was functionally significant, as it diminished inflammatory cytokine production and IgE-mediated FcεRI up-regulation. IL-10 and IL-4 reduced FcεRI β protein expression without altering the α or γ subunits. The ability of IL-4 and IL-10 to alter FcεRI expression by targeting the β-chain, a critical receptor subunit known to modulate receptor expression and signaling, suggests the presence of a Th2 cytokine-mediated homeostatic network that could serve to both initiate and limit mast cell effector function.

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“…In humans, monocytes are the major source for IL-10 production [2,3] with additional amounts being generated by T cells, B cells [4,5], myeloid dendritic cells (DC) [6] and mast cells [7]. Of the T cell subsets, the regulatory T cells are the primary cell types responsible for IL-10 production [8,9].…”

Section: Introductionmentioning

confidence: 99%

Differential interleukin-10 production stratified by −571 promoter polymorphism in purified human immune cells

Steinke¹,

Barekzi²,

Huyett³

et al. 2007

Cellular Immunology

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SummaryA C-to-A base substitution has been identified at bp -571 in the IL-10 promoter and has been linked to numerous diseases. To investigate the role of this polymorphism on IL-10 production, T cells, B cells and monocytes were enriched from peripheral blood from subjects either homozygous for the C or A allele. Treatment of monocytes and B cells with lipopolysaccharide from individuals homozygous for the C allele resulted in higher levels of IL-10 production as compared to monocytes from individuals homozygous for the A allele. Though not statistically significant, when B cells were treated with anti-IgM or T cells with concanavalin A higher levels of IL-10 were produced from individuals homozygous for the A allele. Changes in IL-10 protein production were paralleled by similar changes in IL-10 mRNA production. These results demonstrate that changes in IL-10 production observed due to the -571 genotype depend on both cell type and stimulus.

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Interleukin 10: a novel stimulatory factor for mast cells and their progenitors.

Cited by 486 publications

References 13 publications

IL-19 Induces Production of IL-6 and TNF-α and Results in Cell Apoptosis Through TNF-α

IL-19 Induces Production of IL-6 and TNF-α and Results in Cell Apoptosis Through TNF-α

IL-10 Inhibits FcεRI Expression in Mouse Mast Cells

Differential interleukin-10 production stratified by −571 promoter polymorphism in purified human immune cells

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