0000000000131903

AUTHOR

Robert B. Sim

showing 4 related works from this author

Evidence for auto-reactivity against the collectins, SP-A and MBL, in rheumatoid arthritis synovial fluids: Lack of cross-reactivity with C1q or type…

1997

ChemistryRheumatoid arthritisImmunologyImmunologymedicineType II collagenImmunology and AllergyCollectinReactivity (chemistry)medicine.disease_causemedicine.diseaseCross-reactivityImmunology Letters
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Functional analysis of the classical, alternative, and MBL pathways of the complement system: standardization and validation of a simple ELISA.

2004

Primary defence against invading microorganisms depends on a functional innate immune system and the complement system plays a major role in such immunity. Deficiencies in one of the components of the complement system can cause severe and recurrent infections, systemic diseases, such as systemic lupus erythematosus (SLE) and renal disease. Screening for complement deficiencies in the classical or alternative complement pathways has mainly been performed by haemolytic assays. Here, we describe a simple ELISA-based format for the evaluation of three pathways of complement activation. The assays are based on specific coatings for each pathway in combination with specific buffer systems. We ha…

Innate immune systemSystemic lupus erythematosusImmunologyComplement Pathway AlternativeComplement Pathway Mannose-Binding LectinEnzyme-Linked Immunosorbent AssayComplement System ProteinsBiologyComplement fixation testmedicine.diseaseMannose-Binding LectinComplement systemComplement (complexity)Immune systemImmunologymedicineImmunology and AllergyHumansLupus Erythematosus SystemicComplement Pathway ClassicalReagent Kits DiagnosticFicolinComplement ActivationMannan-binding lectinJournal of immunological methods
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Complement C1q is dramatically up-regulated in brain microglia in response to transient global cerebral ischemia.

2000

Abstract Recent evidence suggests that the pathophysiology of neurodegenerative and inflammatory neurological diseases has a neuroimmunological component involving complement, an innate humoral immune defense system. The present study demonstrates the effects of experimentally induced global ischemia on the biosynthesis of C1q, the recognition subcomponent of the classical complement activation pathway, in the CNS. Using semiquantitative in situ hybridization, immunohistochemistry, and confocal laser scanning microscopy, a dramatic and widespread increase of C1q biosynthesis in rat brain microglia (but not in astrocytes or neurons) within 24 h after the ischemic insult was observed. A marke…

MaleImmunologyIschemiaInflammationIn situ hybridizationBiologySulfur RadioisotopesProinflammatory cytokineRNA ComplementaryCerebrospinal fluidDownregulation and upregulationmedicineImmunology and AllergyAnimalsTransient (computer programming)Rats WistarComplement C1qIn Situ HybridizationPharmacologyMicrogliaComplement C1qBrainRNA Probesmedicine.diseaseImmunohistochemistryCell biologyComplement systemRatsUp-Regulationmedicine.anatomical_structureIschemic Attack TransientImmunologyMicrogliamedicine.symptomNeuroscienceDigoxigeninJournal of immunology (Baltimore, Md. : 1950)
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Humoral autoreactivity directed against surfactant protein-A (SP-A) in rheumatoid arthritis synovial fluids.

2000

SUMMARY SP-A is found principally in the lung, and has been associated with lamellar bodies also found in the synovial joint. Both SP-A and C1q contain collagen-like regions, and SP-A and C1q have some structural similarities, both having a globular head region and a collagen-like tail. Here we are able to show that (i) autoreactivity to SP-A, as expressed by IgG and IgM autoantibodies, is present in synovial fluid (SF) isolated from patients with rheumatoid arthritis (RA); (ii) in absorption experiments only a limited degree of cross-reactivity between autoantibodies reactive with C1q and SP-A is observed; (iii) there is no cross-reactivity between autoantibodies reactive with type II coll…

Pulmonary Surfactant-Associated ProteinsKnee JointProteolipidsImmunologyType II collagenchemical and pharmacologic phenomenamedicine.disease_causeAutoantigensImmunoglobulin GAutoimmunityArthritis RheumatoidRheumatic DiseaseAntigenSynovial jointSynovial FluidmedicineImmunology and AllergySynovial fluidAnimalsHumansskin and connective tissue diseasesAutoantibodiesbiologyPulmonary Surfactant-Associated Protein AChemistryComplement C1qAutoantibodyPulmonary Surfactantsmedicine.anatomical_structureImmunoglobulin MImmunoglobulin MImmunoglobulin GImmunologybiology.proteinBinding Sites AntibodyCollagenPeptidesChickensDimerizationClinical and experimental immunology
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