Interleukin-18

Gracie, J. Alastair; Robertson, Susan; McInnes, Iain B.

doi:10.1189/jlb.0602313

Cited by 638 publications

(539 citation statements)

References 191 publications

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“…Recently, over-secretion of IL-18 by monocytes in patients with primary and secondary HPS has been described. IL-18 is known to be a potent inducer of IFNg and TNFa production by T lymphocytes and NK cells as well as induction of Fas-L expression on lymphocytes, which can mediate cytotoxicity against Fas expressing cells such as hepatocytes [12][13][14][15][16]. As a result, clinical manifestation of HPS such as fever, hepatosplenomegaly, cytopenias, liver dysfunction, and coagulopathy are mostly attributable to hypercytokinemia [6,[8][9][10][11][13][14][15].…”

Section: Discussionmentioning

confidence: 99%

Crimean‐Congo hemorrhagic fever: Five patients with hemophagocytic syndrome

Fışgın

Tanyel

et al. 2007

American J Hematol

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Three pediatric and two adult Turkish patients with Crimean Congo Hemorrhagic Fever (CCHF) induced hemophagocytic syndrome (HPS) were admitted to Ondokuz Mayis University Hospital, which is in the Middle Black Sea Region of Turkey. All of them had remarkable hemophagocytosis in the bone marrow with severe bleeding symptoms along with the other known clinical and laboratory findings of CCHF. We would like to present these patients and to discuss the pathophysiology and the effect of acquired HPS on the severity of the disease. Am. J. Hematol., 2008. © 2007 Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

Crimean‐Congo hemorrhagic fever: Five patients with hemophagocytic syndrome

Fışgın

Tanyel

et al. 2007

American J Hematol

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“…At 24 h after infection with L. major, the IL-12-induced release of IFN-+ was reduced by 80-90% in Tyk2 -/-compared to wild-type lymph node cells. IL-18, which synergizes with endogenously produced or exogenously added IL-12 for the induction of IFN-+ and which does not signal via STAT4 on its own [22], only partially restored the production of IFN-+ by Tyk2 -/-cells ( Fig. 4A and B).…”

Section: Tyk2 Is Required For the Production Of Ifn-+ By Nk Cells Andmentioning

confidence: 96%

“…The lysates (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) ? g protein/lane) were separated by 7.5% SDS-PAGE, transferred to reinforced nitrocellulose (0.45 ?…”

Section: Sds-page Western Blotting and Immunoprecipitationmentioning

confidence: 99%

Control of Leishmania major in the absence of Tyk2 kinase

et al. 2004

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IL‐12 is indispensable for the control of many intracellular pathogens, but the components of the signaling pathway that are essential for its function in vivo are incompletely understood. Here, we investigated in the Leishmania major mouse model whether Tyk2 kinase is required for the generation of a protective immune response. Unlike C57BL/6 controls, Tyk2–/–mice developed severe skin lesions after infection that frequently ulcerated, but ultimately healed. NK cell cytotoxicity was absent in infected Tyk2–/– mice, even after IL‐12 pretreatment, which correlated with a STAT4 activation defect. IFN‐α / β, which was still able to activate STAT1 in Tyk2–/– NK cells, reconstituted their cytotoxic activity, but not their IL‐12responsiveness. The IL‐12‐induced production of IFN‐γ by NK cells and CD8+ T cells was strongly suppressed in Tyk2–/– mice at day 1 of infection, but partly regained during the late phase of infection. Tyk2–/– CD4+ T cells developed into Th1 cells (although in a delayed fashion) and infected Tyk2–/– mice expressed normals levels of inducible NO synthase. Thus, Tyk2 is required for the IL‐12 response of NK cells and CD8+ T cells in L. major‐infected mice, but not for the generation of Th1 cells and the ultimate control of the disease.

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“…Among the cytokines, IL-18 should also be particularly interesting with respect to the pathogenesis of JIA. IL-18 stimulates a variety of inflammatory responses, enhances proliferation and activity of T cells and NK cells, and shifts helper T cell balance towards Th1 response [6,7]. We suspected that IL-18 is not only a prominent mediator of JIA, but that different forms of JIA could be associated with different levels of IL-18 as well.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-18 as a mediator of systemic juvenile idiopathic arthritis

et al. 2006

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The objective of this report is to explore the balance between serum and synovial fluid levels of interleukin (IL)-18 in children with juvenile idiopathic arthritis (JIA).Blood samples were obtained from 81 children with JIA and 18 control children.Synovial fluid samples were collected from 16 children with oligoarticular JIA.Concentrations of IL-18 were determined using commercial kit.Patients with systemic JIA had higher serum levels of IL-18 than patients with other forms of JIA or control children, both during the active (median, range: 6240, 1600 -78750 pg/mL) and inactive (1615, 513 -3270 pg/mL) phase of disease (ANOVA, P<0.05). Levels of IL-18 in sera of children with oligoarticular JIA (255, 89 -4342 pg/mL) were similar to the respective synovial fluid levels (217, 89 -1245 pg/mL).Serum levels of IL-18 were proportional to the erythrocyte sedimentation rate and levels of C-reactive protein, but inversely proportional to the haemoglobin levels.IL-18 appears to be an important mediator of systemic JIA, while it seems of a lesser relevance in pathogenesis of other JIA forms. Therefore, inhibition of IL-18 might be a base for a successful biologic therapy of systemic JIA.

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Interleukin-18

Cited by 638 publications

References 191 publications

Crimean‐Congo hemorrhagic fever: Five patients with hemophagocytic syndrome

Crimean‐Congo hemorrhagic fever: Five patients with hemophagocytic syndrome

Control of Leishmania major in the absence of Tyk2 kinase

Interleukin-18 as a mediator of systemic juvenile idiopathic arthritis

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