Search results for "Interleukin-23 Subunit p19"

showing 2 items of 12 documents

IL-23 receptor regulates unconventional IL-17-producing T cells that control bacterial infections.

2010

AbstractIL-23 plays an important role in autoimmune tissue inflammation and induces the generation of not fully characterized effector cells that mediate protection against pathogens. In this paper, we established the essential role of IL-23R in the host response against intracellular pathogens. IL-23 was critical for the expansion or maintenance of γδ and double negative (DN) αβ T cells. These cells were rapidly recruited to the site of infection and produced large amounts of IL-17, IFN-γ, and TNF-α. Notably, DN T cells transferred into L. monocytogenes-infected RAG2−/− mice prevented bacterial growth, confirming their protective role against intracellular pathogens. Our results show that …

T cellCD8 AntigensReceptors Antigen T-Cell alpha-betaImmunologyMice NudeMice TransgenicBiologyArticleImmunophenotypingInterferon-gammaMiceImmune systemAntigenCell MovementT-Lymphocyte SubsetsmedicineImmunology and AllergyAnimalsInterferon gammaListeriosisCells CulturedMice KnockoutEffectorTumor Necrosis Factor-alphaIntracellular parasiteInterleukin-17Receptors Antigen T-Cell gamma-deltaReceptors InterleukinCoculture TechniquesCell biologymedicine.anatomical_structureImmunologyCD4 AntigensInterleukin-23 Subunit p19Tumor necrosis factor alphaInterleukin 17Peritoneummedicine.drugJournal of immunology (Baltimore, Md. : 1950)
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Cutting Edge: IL-23 Cross-Regulates IL-12 Production in T Cell-Dependent Experimental Colitis

2006

Abstract Although IL-12 and IL-23 share the common p40 subunit, IL-23, rather than IL-12, seems to drive the pathogenesis of experimental autoimmune encephalomyelitis and arthritis, because IL-23/p19 knockout mice are protected from disease. In contrast, we describe in this study that newly created LacZ knockin mice deficient for IL-23 p19 were highly susceptible for the development of experimental T cell-mediated TNBS colitis and showed even more severe colitis than wild-type mice by endoscopic and histologic criteria. Subsequent studies revealed that dendritic cells from p19-deficient mice produce elevated levels of IL-12, and that IL-23 down-regulates IL-12 expression upon TLR ligation. …

T-LymphocytesTransgeneT cellImmunologyDown-RegulationMice TransgenicInterleukin-23PathogenesisMiceInterleukin 23AnimalsImmunology and AllergyMedicineColitisCells Culturedbusiness.industryInterleukinsExperimental autoimmune encephalomyelitisColitismedicine.diseaseInterleukin-12Survival RateDisease Models AnimalProtein Subunitsmedicine.anatomical_structureImmunologyKnockout mouseInterleukin-23 Subunit p19Interleukin 12Disease SusceptibilitybusinessThe Journal of Immunology
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