0000000000276692

AUTHOR

J. Alsenz

showing 4 related works from this author

The critical concentration of C1-esterase inhibitor (C1-INH) in human serum preventing auto-activation of the first component of complement (C1)

2005

C1-esterase inhibitor (C1-INH) was depleted from normal human serum (NHS) at 4 degrees C by affinity chromatography with a monoclonal anti-C1-INH antibody (mAb 13 E1) coupled to CNBr-activated Sepharose 4B. The C1-INH-depleted serum (C1-INH-depl-HS) had normal levels of C1, C4, and CH 50 and C1-INH concentration was less than 10% of normal (15 microg/ml in C1-INH-depl-HS compared to 230 microg/ml in NHS). C1-auto-activation in C1-INH-depl-HS was followed by measuring C4-consumption in a haemolytic assay and by detection of activated C1s in a C1s-ELISA. After a lag phase of 10-20 min, C1-auto-activation in C1-INH depl-HS occurred and reached its maximum after 40 min at 37 degrees C. In contr…

Serummedicine.drug_classImmunologyComplement C1 Inactivator ProteinsMonoclonal antibodyNeutralizationSepharoseMiceAffinity chromatographyComplement C1medicineAnimalsHumansheterocyclic compoundsMolecular BiologybiologyChemistryAntibodies Monoclonalbiochemical phenomena metabolism and nutritionrespiratory systembacterial infections and mycosesMolecular biologyrespiratory tract diseasesC1 esteraseComplement C1 Inactivator ProteinsBiochemistryMonoclonalbiology.proteinAntibodyMolecular Immunology
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Acquired C1 inhibitor (C1-INH) deficiency type II. Replacement therapy with C1-INH and analysis of patients' C1-INH and anti-C1-INH autoantibodies

1989

Abstract The response of two patients with autoantibody-mediated C1-inhibitor (C1-INH) deficiency to replacement therapy with C1-INH was studied over a period of 3 d. In patient 1 an acute attack of angioedema was successfully managed by infusion of 1,000 U of C1-INH concentrate. C1-INH function returned to normal levels within 30 min, while CH50 and C4 peaked after 6-7 h and C1 hemolytic activity reached 50-60% of normal after 3 d. Immediately after the injection an increase in C1-INH-anti-C1-INH complexes was observed. Based on NH2-terminal sequence analysis of the patients' Mr 96,000 C1-INH, it is concluded that this fragment is generated after cleavage of C1-INH in its active site by on…

Molecular Sequence DataPharmacologyComplement C1 Inactivator ProteinsEpitopeC1-inhibitorAutoimmune DiseasesAntibody SpecificityImmunopathologyBlood plasmamedicineHumansheterocyclic compoundsAmino Acid SequenceAngioedemaInfusions IntravenousAutoantibodiesAngioedemabiologybusiness.industryAutoantibodyAntibody titerGeneral Medicinebiochemical phenomena metabolism and nutritionrespiratory systembacterial infections and mycosesrespiratory tract diseasesImmunologybiology.proteinmedicine.symptomAntibodybusinessResearch Article
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Importance of Factors H and I for the Adherence of C3b-Coated Erythrocytes to Cells

1983

Abstract The role of cell membrane-associated human factor H for the binding of cell-bound Cab to complement receptor-carrying (CR + ) cells was investigated. Pretreatment of CR + cells with antibodies to factor H inhibited the adherence of Cab-coated red cells to human tonsil lymphocytes (TL) and peripheral blood monocytes (Mo). The Cab receptor reactivity of human polymorphonuclear leucocytes (PMN) was not influenced and the one of Raji lymphoblastoid cells only slightly influenced; iC3b and Cad receptor reactivity was in no case affected. When diisopropylfluorophosphate (DFP) in a concentration of 0.1 mM was present during pretreatment of the CR + cells with anti H, the antibodies gained…

ErythrocytesIsoflurophateRosette Formationmedicine.drug_classLymphocyteComplement Pathway AlternativeImmunologyMonoclonal antibodyMonocytesImmunoglobulin Fab FragmentsComplement C3b Inactivator ProteinsmedicineAnimalsHumansImmunology and AllergyLymphocytesComplement ActivationbiologyChemistryLymphoblastfungifood and beveragesHematologyMolecular biologyReceptors ComplementComplement systemRaji cellmedicine.anatomical_structureBiochemistryComplement Factor HFactor HReceptors Complement 3bbiology.proteiniC3bRabbitsAntibodyImmunobiology
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The Clinical Enzymology of the Complement System

1989

The complement (C) system is one of the most important humoral systems mediating many activities that contribute to inflammation and host defense, e.g. various anaphylatoxin activities, Chemotaxis and opsonization for phagocytosis. The C system is similar to other humoral systems, such as coagulation, fibrinolysis and the kinin system, a multifactoral system whose activation represents sequentially occurring multi-step activation cascades of the “classical” as well as the “alternative” pathway.

Antibody opsonizationClassical complement pathwayChemistrymedicineAnaphylatoxinChemotaxisInflammationKininComplement deficiencymedicine.symptommedicine.diseaseCell biologyComplement system
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