Quantitation of the anaphylatoxin C3a in the presence of C3 by a novel sandwich ELISA using monoclonal antibody to a C3a neoepitope

Zilow, G.; Naser, W.; Rutz, R.; Bürger, Reinhard

doi:10.1016/0022-1759(89)90169-5

Cited by 24 publications

(10 citation statements)

References 15 publications

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“…Concentration of plasma C3 was determined by radial immunodiffusion (Behring Diagnostics, Frankfurt, Germany). C3a-desArg was quantitated as previously described (20). Briefly, wells of polystyrene microtiter plates (Nunc, Roskilde, Denmark) were incubated with 100 pL of purified MAb H466 (10 pg/mL) in 0.01 M sodium phosphate, 0.15 M NaCI, pH 7.4 (buffer A).…”

Section: Methodsmentioning

confidence: 99%

Complement Activation in Newborn Infants with Early Onset Infection

Zilow

Bürger

et al. 1993

Pediatr Res

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Section: Methodsmentioning

confidence: 99%

Complement Activation in Newborn Infants with Early Onset Infection

Zilow

Bürger

et al. 1993

Pediatr Res

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“…C3a-desArg levels were determined as previously described in an ELISA system using a monoclonal antibody to a neoantigenic epitope of C3a-desArg. 30,31 Control experiments Heat-aggregated IgG (HAAG) was generated according to standard techniques. In brief, 15 mg/ml human IgG in PBS (Dianova) were heated for 30 min at 63°C.…”

Section: Complement Studiesmentioning

confidence: 99%

Complement activation by recombinant adenoviruses

et al. 2001

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“…C3a was determined by ELISA (Progen, Heidelberg, FRG) as described by Zilow et al [16] using a monoclonal antibody to C3a ncoantigen.…”

Section: C3a Enzyme Immunoassaymentioning

confidence: 99%

Complement Activation by House Dust: Reduced Reactivity of Serum Complement in Patients with Bronchial Asthma

Castro

Schmitz-Schumann

Rother

et al. 1991

Int Arch Allergy Immunol

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Among ten different allergens, house-dust extract proved to be the most potent complement activator. It was therefore chosen to investigate the susceptibility of complement in the serum and bronchoalveolar lavage fluid of patients with extrinsic asthma and control persons. Complement activation in serum was assessed by the appearance of C3d as well as the activation-specific protein-protein complexes C1rs-C1inhibitor (classical pathway) and C3b(Bb)P (alternative pathway). Complement was activated via both the classical and the alternative pathway in a dose- and time-dependent manner. In contrast to earlier observations, however, complement was less affected in the serum of asthmatics than in the serum of normal individuals. Differences were restricted to alternative-pathway activation, probably due to preactivation and/or a significantly higher serum concentration of the regulatory protein factor H in asthmatic patients. In vitro generation of C3a in bronchoalveolar lavage fluid could not be achieved, although the presence of alternative pathway proteins C3, B and D was demonstrated.

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Quantitation of the anaphylatoxin C3a in the presence of C3 by a novel sandwich ELISA using monoclonal antibody to a C3a neoepitope

Cited by 24 publications

References 15 publications

Complement Activation in Newborn Infants with Early Onset Infection

Complement Activation in Newborn Infants with Early Onset Infection

Complement activation by recombinant adenoviruses

Complement Activation by House Dust: Reduced Reactivity of Serum Complement in Patients with Bronchial Asthma

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