Mast cells produce interleukin-25 upon FcεRI-mediated activation

Ikeda, Kei; Nakajima, Hiroshi; Suzuki, Kotaro; Kagami, Shin-ichiro; Hirose, Koichi; Suto, Akira; Saitō, Yasushi; Iwamoto, Itsuo

doi:10.1182/blood-2002-09-2817

Cited by 223 publications

(175 citation statements)

References 12 publications

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“…Although the source of IL-25 has not been fully elucidated, it can be produced by a number of cell populations. While we did not detect IL-25 in bone marrow-derived mast cells stimulated with SCF, they have been described to produce IL-25 by other stimuli (44). A recent study has suggested that epithelial cells produce IL-25 in response to innate signals from allergens (22).…”

Section: Gr1contrasting

confidence: 44%

Pulmonary IL-17E (IL-25) Production and IL-17RB+ Myeloid Cell-Derived Th2 Cytokine Production Are Dependent upon Stem Cell Factor-Induced Responses during Chronic Allergic Pulmonary Disease

Dolgachev

Petersen

Budelsky

et al. 2009

The Journal of Immunology

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In the present studies local neutralization of allergen-induced stem cell factor (SCF) leads to decreased production of Th2 cytokines, a reduction in inflammation, allergen-specific serum IgE/IgG1, and attenuation of severe asthma-like responses. The local blockade of pulmonary SCF also resulted in a significant reduction of IL-17E (IL-25). Sorted cell populations from the lung indicated that IL-25 was produced from c-kit+ cells, whereas Th2 cytokine production was primarily from c-kit− cell populations. SCF stimulated c-kit+ eosinophils produced IL-25, whereas bone marrow-derived mast cells did not. Using 4get mice that contain a IL-4-IRES-eGFP that when transcribed coexpress GFP and IL-4, our studies identified cells that comprised a CD11b+, GR1+, Ly6C+/−, c-kit−, CD4−, CD11c−, MHC class IIlow cell population as a source of IL-4 in the lung after chronic allergen challenge. In the bone marrow a similar cell was identified with approximately a third of the IL-4+ cells also expressing c-kit+. The pulmonary and bone marrow IL-4+ cell populations were significantly reduced upon local pulmonary anti-SCF treatment. Subsequently, when IL-25R was examined during the chronic allergen responses the expression was found on the IL-4+ myeloid cell population that expressed CD11b+GR1+. Interestingly, the IL-25R+ cells in the bone marrow were also all CD11b+GR1+, similar to the lung cells, but they were also all c-kit+, potentially suggesting a maturation of the bone marrow cell once it enters the lung and/or is stimulated by SCF. Overall, these studies suggest a complex relationship between SCF, bone marrow-derived IL-25-responsive myeloid cells, Th2 cytokines, and chronic allergic disease.

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Section: Gr1contrasting

confidence: 44%

Pulmonary IL-17E (IL-25) Production and IL-17RB+ Myeloid Cell-Derived Th2 Cytokine Production Are Dependent upon Stem Cell Factor-Induced Responses during Chronic Allergic Pulmonary Disease

Dolgachev

Petersen

Budelsky

et al. 2009

The Journal of Immunology

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“…IL-25 is expressed in Th2-polarized CD4 ϩ T cells (2) and activated mast cells (34). It has also been reported that in vivo administration of IL-25 promotes the expression of Th2-cell associated cytokines such as IL-4, IL-5, and IL-13 from a non-T/non-B cell population (2,4).…”

Section: Discussionmentioning

confidence: 99%

Involvement of TNF Receptor-Associated Factor 6 in IL-25 Receptor Signaling

Maezawa

Nakajima

Suzuki

et al. 2006

The Journal of Immunology

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IL-25 (IL-17E) induces IL-4, IL-5, and IL-13 production from an unidentified non-T/non-B cell population and subsequently induces Th2-type immune responses such as IgE production and eosinophilic airway inflammation. IL-25R is a single transmembrane protein with homology to IL-17R, but the IL-25R signaling pathways have not been fully understood. In this study, we investigated the signaling pathway under IL-25R, especially the possible involvement of TNFR-associated factor (TRAF)6 in this pathway. We found that IL-25R cross-linking induced NF-κB activation as well as ERK, JNK, and p38 activation. We also found that IL-25R-mediated NF-κB activation was inhibited by the expression of dominant negative TRAF6 but not of dominant negative TRAF2. Furthermore, IL-25R-mediated NF-κB activation, but not MAPK activation, was diminished in TRAF6-deficient murine embryonic fibroblast. In addition, coimmunoprecipitation assay revealed that TRAF6, but not TRAF2, associated with IL-25R even in the absence of ligand binding. Finally, we found that IL-25R-mediated gene expression of IL-6, TGF-β, G-CSF, and thymus and activation-regulated chemokine was diminished in TRAF6-deficient murine embryonic fibroblast. Taken together, these results indicate that TRAF6 plays a critical role in IL-25R-mediated NF-κB activation and gene expression.

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“…However, IL-25 biological activities appear to markedly differ from those shown by its fellow members as it favors promotion of Th2-associated cytokines (8). IL-25 is reported to be produced by Th2 and mast cells (8,9). IL-25 was also shown to induce production of pro-inflammatory chemokine IL-8 and to activate NF-B1 (10).…”

Section: Introductionmentioning

confidence: 99%