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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 20 May 2015.

Interleukin 25

IL-25, IL-17E, Interleukin-25
The protein encoded by this gene is a cytokine that shares sequence similarity with interleukin 17. This cytokine can induce NF-kappaB activation, and stimulate the production of interleukin 8. Both this cytokine and interleukin 17B are ligands for the cytokine receptor IL17BR. Studies of a similar gene in mice suggest that this cytokine may be a pro-inflammatory cytokine favoring the Th2-type immune response. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Mar 2010] (from NCBI)
Top mentioned proteins: TH2, IL-17, IL-13, IL-33, IL-4
Papers on IL-25
TNF-related apoptosis-inducing ligand (TRAIL) regulates midline-1, thymic stromal lymphopoietin, inflammation, and remodeling in experimental eosinophilic esophagitis.
New
Mattes et al., Newcastle, Australia. In J Allergy Clin Immunol, 13 Jun 2015
This was associated with reduced expression of CCL24, CCL11, CCL20, IL-5, IL-13, IL-25, TGFB, and TSLP.
Vitamins A and D have antagonistic effects on expression of effector cytokines and gut-homing integrin in human innate lymphoid cells.
New
Shreffler et al., Boston, United States. In Clin Exp Allergy, 08 Jun 2015
ILC1, ILC2, and ILC3 cells were cultured for 5 days with RA, 1,25D3, and various cytokines known to activate ILCs (IL-2, IL-7, IL-12, thymic stromal lymphopoietin (TSLP), IL-25, and IL-33).
Diverse Inflammatory Cytokines Induce Selectin Ligand Expression on Murine CD4 T Cells via p38α MAPK.
New
Kansas et al., Chicago, United States. In J Immunol, 04 Jun 2015
Among 20 cytokines that affect Th cell differentiation, we identified six that induce expression of selectin ligands on murine CD4 T cells above the low levels associated with TCR engagement: IL-12, IL-18, IL-27, IL-9, IL-25, and TGF-β1.
Interleukin-25 and interleukin-33 as mediators of eosinophilic inflammation in chronic rhinosinusitis.
New
Harvey et al., Sydney, Australia. In Am J Rhinol Allergy, 31 May 2015
METHOD: Sinus mucosal samples from patients with CRS who were undergoing sinus surgery as part of their management were analyzed for IL-25, IL-33, and TSLP messenger RNA (mRNA) expression by quantitative polymerase chain reaction.
Interleukin-17B Antagonizes Interleukin-25-Mediated Mucosal Inflammation.
New
Impact
Dong et al., Chicago, United States. In Immunity, 21 May 2015
Among them, IL-25 has been shown to be important in allergic inflammation and protection against parasitic infection.
At the bedside: the emergence of group 2 innate lymphoid cells in human disease.
Review
New
Peebles, Nashville, United States. In J Leukoc Biol, Mar 2015
Likewise, selectively and completely inhibiting ILC2 activation is also not currently possible, as several activating cytokines, IL-25, IL-33, and TSLP, act in redundancy or are not specific for ILC2 stimulation.
At the bench: understanding group 2 innate lymphoid cells in disease.
Review
New
Doherty, San Diego, United States. In J Leukoc Biol, Mar 2015
ILC2s were described initially as lineage-negative lymphocytes that produce high levels of Th2 cytokines IL-5 and IL-13 in response to IL-25 and IL-33 and promote protection against helminth infections.
Epithelial cytokines and pulmonary allergic inflammation.
Review
New
Saglani et al., London, United Kingdom. In Curr Opin Immunol, Mar 2015
UNASSIGNED: The triad of epithelial derived cytokines, IL-25, IL-33 and TSLP are important for the initiation and development of pulmonary immune responses to environmental stimuli.
IL-25-responsive, lineage-negative KLRG1(hi) cells are multipotential 'inflammatory' type 2 innate lymphoid cells.
New
Impact
Paul et al., Bethesda, United States. In Nat Immunol, Feb 2015
We report the existence of an inflammatory ILC2 (iILC2) population responsive to interleukin 25 (IL-25) that complemented IL-33-responsive natural ILC2 (nILC2) cells.
Group 2 Innate Lymphoid Cells in Health and Disease.
Review
New
Artis et al., New York City, United States. In Cold Spring Harb Perspect Biol, Feb 2015
The epithelial cell-derived cytokines IL-25, IL-33, and TSLP regulate the activation and effector functions of ILC2s, and recent studies suggest that their responsiveness to these cytokines and other factors may depend on their tissue environment.
Interleukin-17 in human inflammatory diseases.
Review
New
Shahneh et al., Tehrān, Iran. In Postepy Dermatol Alergol, Aug 2014
Recently discovered related molecules are forming a family of cytokines, the IL-17 family, IL-17A, IL-17B, IL-17C, IL-17D, IL-17E and IL-17F.
Chitin activates parallel immune modules that direct distinct inflammatory responses via innate lymphoid type 2 and γδ T cells.
New
Impact
Locksley et al., San Francisco, United States. In Immunity, Apr 2014
We show that inhaled chitin induced expression of three epithelial cytokines, interleukin-25 (IL-25), IL-33, and thymic stromal lymphopoietin (TSLP), which nonredundantly activated resident innate lymphoid type 2 cells (ILC2s) to express IL-5 and IL-13 necessary for accumulation of eosinophils and alternatively activated macrophages (AAMs).
Genetic deletion of IL-25 (IL-17E) confers resistance to dextran sulfate sodium-induced colitis in mice.
Zhao et al., Baltimore, United States. In Cell Biosci, 2013
BACKGROUND: IL-25 is emerging as a key regulator of inflammation in the intestinal mucosa because of its ability to promote type 2 while suppressing Th1 and Th17 responses.
An ACT1 mutation selectively abolishes interleukin-17 responses in humans with chronic mucocutaneous candidiasis.
Impact
Casanova et al., New York City, United States. In Immunity, 2013
The patients' fibroblasts failed to respond to IL-17A and IL-17F, and their T cells to IL-17E.
TH2, allergy and group 2 innate lymphoid cells.
Review
Impact
Flavell et al., New Haven, United States. In Nat Immunol, 2013
The initiation of type 2 immune responses by the epithelial cell-derived cytokines IL-25, IL-33 and TSLP has been an area of extensive research in the past decade.
Epithelial cell-specific Act1 adaptor mediates interleukin-25-dependent helminth expulsion through expansion of Lin(-)c-Kit(+) innate cell population.
Impact
GeneRIF
Li et al., Cleveland, United States. In Immunity, 2012
Th2 cell-inducing cytokine (IL-25) expression were reduced in the intestinal epithelial cells from the infected and IL-25-injected epithelial-specific Act1-deficient mice.
Interleukin-25 induces type 2 cytokine production in a steroid-resistant interleukin-17RB+ myeloid population that exacerbates asthmatic pathology.
Impact
GeneRIF
Lukacs et al., Ann Arbor, United States. In Nat Med, 2012
data establish IL-25 and its receptor IL-17RB as targets for innate and adaptive immune responses in chronic allergic airway disease and identify T2M cells as a new steroid-resistant cell population
The involvement of inflammatory cytokines in the pathogenesis of recurrent miscarriage.
GeneRIF
Emanuelli et al., Ancona, Italy. In Cytokine, 2012
We observed significant downregulation of IL-25 in women with recurrent miscarriage compared with controls.
IL-22 attenuates IL-25 production by lung epithelial cells and inhibits antigen-induced eosinophilic airway inflammation.
GeneRIF
Nakajima et al., Chiba, Japan. In J Allergy Clin Immunol, 2011
IL-22 attenuates antigen-induced airway inflammation, possibly by inhibiting IL-25 production by lung epithelial cells.
T cell-derived Act1 is necessary for IL-25-mediated Th2 responses and allergic airway inflammation.
GeneRIF
Li et al., Cleveland, United States. In J Immunol, 2011
findings indicate that Act1 expression in T cells is required for cellular and humoral Th2-mediated allergic responses and the development of airway hyperresponsiveness, in part, through Act1's function in IL-25-induced development of Th2 T cells
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