0000000000860557

AUTHOR

E. Giardina

showing 3 related works from this author

Glucose-induced loss of glycosyl-phosphatidylinositol-anchored membrane regulators of complement activation (CD59, CD55) by in vitro cultured human u…

2000

Aims/hypothesis. This study examines whether increased glucose concentrations are responsible for a decreased expression of membrane regulators of complement activation molecules. The effect of high glucose in determining an increase in membrane attack complex deposition on endothelial cells was also investigated. Methods. Endothelial cells were isolated from umbilical cord tissue, cultured in the presence of increased concentrations of glucose, and the expression of CD46, CD55, and CD59 was detected by ELISA (enzyme-linked immunosorbent assay) and by flow cytometry. Glucose-treated endothelial cells were also incubated with antiendothelial cell antibodies and fresh complement to assess the…

medicine.medical_specialtyUmbilical VeinsEndotheliumGlycosylphosphatidylinositolsEndocrinology Diabetes and MetabolismCellCD59 AntigensCD59Complement Membrane Attack ComplexBiologyUmbilical veinMembrane Cofactor ProteinAntigens CDPregnancyInternal medicineInternal MedicinemedicineHumansComplement ActivationCells CulturedMembrane GlycoproteinsCD55 AntigensCD46Cell biologyComplement systemEndothelial stem cellEndocrinologymedicine.anatomical_structureGlucoseFemaleEndothelium VascularComplement membrane attack complexDiabetologia
researchProduct

Overexpression of interleukin-23, but not interleukin-17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis

2009

Objective Subclinical gut inflammation is common in spondylarthritis, but the immunologic abnormalities underlying this process are undefined. Perturbation of the interleukin-23 (IL-23)/Th17 axis has emerged as a fundamental trigger of chronic inflammation. This study was undertaken to investigate the expression and tissue distribution of IL-23/Th17–related molecules in Crohn's disease (CD) and in subclinical gut inflammation in ankylosing spondylitis (AS). Methods Quantitative gene expression analysis of Th1/Th2 and IL-23/Th17 responses was performed in intestinal biopsy samples obtained from 12 patients with CD, 15 patients with AS, and 13 controls. IL-23 tissue distribution and identific…

AdultMalePaneth Cellschronic inflammationPathologymedicine.medical_specialtyImmunologyGene ExpressionInflammationMonocytesTh2 CellsRheumatologyIntestinal mucosaIleumankylosing spondylitisPrevalencemedicineInterleukin 23HumansImmunology and Allergyinterleukin-23 (IL-23); Th 17;chronic inflammation; Crohn's disease; ankylosing spondylitisSpondylitis AnkylosingPharmacology (medical)IleitisRNA MessengerIntestinal MucosaSpondylitisinterleukin-23 (IL-23)Subclinical infectionAnkylosing spondylitisbusiness.industryInterleukin-17IleitisMiddle AgedTh1 Cellsmedicine.diseaseUp-RegulationCrohn's diseaseSTAT1 Transcription FactorTh 17ImmunologyInterleukin-23 Subunit p19FemaleInterleukin 17medicine.symptombusinessArthritis & Rheumatism
researchProduct

Two-site ELISA for quantification of the terminal C5b-9 complement complex in plasma

1993

Abstract A quantitative ELISA procedure using monoclonal and polyclonal antibodies against neoantigens of the terminal C5b-9 complement complex has been developed. The ELISA was demonstrated to be both sensitive and reproducible. The normal range for C5b-9 determinations, defined as 2.5–97.5% interval of the values obtained in 76 healthy blood donors, was 3.12–10.3 AU/ml. The presence of rheumatoid factor did not affect the determination of C5b-9 as demonstrated by immunoabsorption studies.

Anticorps monoclonalbiologymedicine.drug_classChemistryImmunologychemical and pharmacologic phenomenaMonoclonal antibodyMolecular biologyfemale genital diseases and pregnancy complicationsPolyclonal antibodiesparasitic diseasesMonoclonalmedicinebiology.proteinImmunology and AllergyRheumatoid factorComplement membrane attack complexQuantitative analysis (chemistry)Normal rangeJournal of Immunological Methods
researchProduct