0000000000155372

AUTHOR

Kiefer R

showing 2 related works from this author

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

2017

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, …

0301 basic medicine030204 cardiovascular system & hematologylaw.invention0302 clinical medicinec-reactive proteinRandomized controlled triallawCardiovascular Diseasemiddle ageddouble-blind methodantibodiesMyocardial infarctionhumansStrokeinterleukin-1betabiologyAntibodies MonoclonaldrugGeneral MedicineLipidAged; anti-inflammatory agents; antibodies; monoclonal; antibodies; monoclonal; humanized; atherosclerosis; c-reactive protein; cardiovascular diseases; dose-response relationship; drug; double-blind method; female; humans; incidence; infections; interleukin-1beta; lipids; male; middle aged; myocardial infarction; neutropenia; secondary prevention; strokestrokeAnti-Inflammatory AgentagedEditorialfemalemyocardial infarctionAtherosclerosiMonoclonalsecondary preventionHumanmedicine.drugmedicine.medical_specialtymonoclonalNeutropeniaAntibodies Monoclonal HumanizedInfectionsPlaceboaged; anti-inflammatory agents; antibodies monoclonal; atherosclerosis; c-reactive protein; cardiovascular diseases; dose-response relationship drug; double-blind method; female; humans; incidence; infection; interleukin-1beta; lipids; male; middle aged; myocardial infarction; neutropenia; secondary prevention; stroke; medicine (all)anti-inflammatory agentsdose-response relationshiplipids03 medical and health sciencesmaleInternal medicinemedicineneutropeniamedicine (all)Dose-Response Relationship Drugbusiness.industryAntiinflammatory Therapy Canakinumab for Atherosclerotic DiseaseC-reactive proteinmedicine.diseaseinfectioncardiovascular diseasesSurgeryCanakinumab030104 developmental biologyincidencebiology.proteinatherosclerosisbusinessNew England journal of medicine
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The PTPN22gain-of-function+1858T(+) genotypes correlate with low IL-2 expression in thymomas and predispose to myasthenia gravis

2009

Protein tyrosine phosphatase, non-receptor type 22 (PTPN22) inhibits T-cell activation and interleukin-2 (IL-2) production. The PTPN22(gain-of-function)+1858T(+) genotypes predispose to multiple autoimmune diseases, including early-onset (non-thymomatous) myasthenia gravis (MG). The disease association and the requirement of IL-2/IL-2 receptor signaling for intrathymic, negative T-cell selection have suggested that these genotypes may weaken T-cell receptor (TCR) signaling and impair the deletion of autoreactive T cells. Evidence for this hypothesis is missing. Thymoma-associated MG, which depends on intratumorous generation and export of mature autoreactive CD4(+) T cells, is a model of au…

AdultMalemedicine.medical_specialtyThymomaAdolescentGenotypeThymomaImmunologyBiologymedicine.disease_causePolymorphism Single NucleotideWhite PeopleAutoimmunityPTPN22Young AdultAntigens CDInternal medicineMyasthenia GravisCentral tolerance inductionGeneticsmedicineHumansCTLA-4 AntigenGenetic Predisposition to DiseaseReceptorGenetics (clinical)AgedAged 80 and overT-cell receptorProtein Tyrosine Phosphatase Non-Receptor Type 22Thymus NeoplasmsMiddle Agedmedicine.diseaseMyasthenia gravisEndocrinologyImmunologyInterleukin-2FemaleCentral toleranceGenes & Immunity
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