Disease relevance of CGN1

• Two complement-dependent assays for circulating immune complexes, the C1q-binding assay and the conglutinin binding, were used to study patients with suspected immune-complex disease [1].
• Forty-one patients with progressive systemic sclerosis were studied for the presence of immune complexes by the fluid- and solid-phase C1q binding, C1 activation, and the fluid-phase conglutinin assays [2].
• The incidence of positive conglutinin binding assays became significantly higher during the course of infective endocarditis (53 percent) than during the course of nonseptic fever (21 percent), but, upon admission, this difference was not significant [3].
• MBP and conglutinin have been shown previously to bind to influenza viruses and to inhibit the infectivity and haemagglutinating activity of influenza viruses [4].
• The conglutinin binding assay which allows quantitation of C3bi-bearing immune complexes was used for 82 patients with hemophilia A [5].

Psychiatry related information on CGN1

• We tested the presence of circulating immune complexes (CIC) in the sera from dementia and Down's syndrome (DS) patients and age-matched controls using two methods: Clq-binding Elisa (ClqB-Elisa) and conglutinin-binding Elisa (KgB-Elisa) [6].

High impact information on CGN1

• We have previously reported that related mammalian serum lectins (mannose-binding lectin [MBL] and conglutinin) have similar effects [7].
• The mannose-binding proteins, pulmonary surfactant apoproteins A and D and conglutinin all qualify as members of this family, whose function appears to be as pattern recognition molecules involved in the first line of defense in the pre-immune host [8].
• Second, the binding to the C3-derived glycoprotein iC3b appears to be exclusively mediated through the Man8 or Man9 oligosaccharide on the alpha chain; there is no evidence for other N-linked oligosaccharides on C3 that are uniquely bound by conglutinin [9].
• Conglutinin and mannan-binding protein are serum proteins that have similar carbohydrate binding specificities toward high mannose-type oligosaccharides, and yet only conglutinin binds the complement glycoprotein iC3b, which contains oligosaccharides of this type [9].
• First, the interaction of conglutinin is profoundly influenced by the state of the protein moiety of the alpha chain in the vicinity of the glycosylation site Asn-917 [9].

Chemical compound and disease context of CGN1

• Immune-complex measurements used 4 established and sensitive techniques (Raji cell assay, fluid and solid-phase C1q assays and conglutinin-binding assay) and a 5th newly devised technique based on the binding of polyethylene-glycol-precipitated immune-complex-rich serum fractions to Staphylococcus aureus [10].

Biological context of CGN1

• We have also examined the fate of C3 on these Salmonellae by measuring the size and quantity of 125I-C3 breakdown fragments by SDS-PAGE, and have determined the kinetics of conversion of C3b to iC3b by using conglutinin, a molecule that binds specifically to iC3b [11].
• The amino acid sequences deduced from both clones (415 and 418 residues; 47.4 and 47.8 kd) showed greater than 50% identity with major peanut (Ara h 1) and soybean (conglutinin subunits) allergens belonging to the vicilin family [12].
• The presence of the glucose moiety in 5% of the human C3 glycoprotein suggests that this glycosylation site is sequestered within the protein and is consistent with previous studies identifying a cryptic conglutinin binding site on C3 that becomes exposed upon its conversion to iC3b [13].
• Both the IC VLDL and IC LDL contained IgG and behaved as IC in the Clq deviation test, platelet aggregation and rheumatoid factor inhibition assays, but not in the conglutinin and Clq binding assays and the Clq solid phase assay [14].
• Immune clearance and in vitro phagocytosis was normal in both patients and not related to their levels of immune complexes (as measured by ELISA C1q and Conglutinin solid-phase binding assay) [15].

Anatomical context of CGN1

• Neither pneumococcal cell wall C3b nor capsular C3b was converted efficiently to a conglutinin-binding form by serum incubation [16].
• Conglutinin is a serum lectin of the innate immune system, which binds high mannose N-glycans when these are appropriately presented on proteins [17].
• However, RA synovial fluids did contain other complexes as shown by the presence of complement consuming activity, C1q binding material and immunoglobulin attaching to conglutinin [18].
• Bacterial aggregating and conglutinin-like factors in human saliva and amniotic fluid: investigations of molecular size [proceedings] [19].
• Conglutinin-like factors and agglutinins for sensitized sheep erythrocytes in parotid and whole saliva from seven subjects were examined [20].

Associations of CGN1 with chemical compounds

• Differential recognition by conglutinin and mannan-binding protein of N-glycans presented on neoglycolipids and glycoproteins with special reference to complement glycoprotein C3 and ribonuclease B [9].
• In addition, C3bi was deposited in a calcium-dependent way onto the insolubilized IgE as shown by the agglutination of latex by conglutinin [21].
• For conglutinin, as for MBP, the best inhibitor was N-acetylglucosamine [22].
• A new method for the detection of circulating immune complexes using radiolabelled conglutinin as a marker for complement-bound complexes precipitated in low concentrations (3.5%) of polyethylene glycol is described [23].
• Binding of immune complexes, purified by sedimentation on sucrose gradient, to conglutinin was inhibited by the presence of T. vulgaris antigen; thus suggesting that this antigen might be present in the complexes [24].

Physical interactions of CGN1

• Third, although conglutinin shows a more restricted binding relative to mannan-binding protein toward the oligosaccharides free of protein, it has a broader binding pattern toward the oligosaccharides as presented on C3-derived glycoproteins [9].
• We studied serum IgA as antibodies to dietary antigens (Ag), as lectin-binding molecules, and as conglutinin-binding immune complexes (IgAIC) in people from geographical areas in which IgA nephropathy (IgAGN) is particularly frequent [25].
• The characteristics of the solid-phase conglutinin method for the isolation of C3-containing complexes from the synovial effusions of rheumatoid arthritis patients were assessed [26].

Regulatory relationships of CGN1

• In the case of MBL the opsonization can be further enhanced by complement activation via the MBLectin pathway while conglutinin interacts with the complement system by binding to the complement degradation product iC3b [27].

Other interactions of CGN1

• Hence, although replacement of the neck recognition domains and CRDs of SP-D with those of MBL and conglutinin conferred increased viral binding activity, it did not favorably affect bacterial binding activity, suggesting that requirements for optimal collectin binding to influenza virus and bacteria differ [28].
• With the conglutinin-binding assay, immune complexes were found in a similar frequency for patients with and without IgA nephropathy [29].
• The best predictors of the final hypothyroid state were female sex, initial hypothyroidism, IgG thyroglobulin antibodies by EIA, and IgG circulating immune complexes assayed by conglutinin-binding test-EIA [30].
• Thus there are no perceptible differences between the RNase protein forms that could account for differential availability of the N-glycan for conglutinin-binding [17].
• Six tests for circulating immune complexes (CIC) developed in four laboratories and representing four main principles [affinity of human platelets, Clq, of RF for aggregated IgG, and of conglutinin (Kg) for complex-bound C3] were evaluated on series of SLE and definite RA [31].

Analytical, diagnostic and therapeutic context of CGN1

• Circulating immune complexes were determined with the 125I-Clq binding assay and the conglutinin binding assay in a prospective, longitudinal study of 40 patients with infective endocarditis, 34 patients with endocardial defects and nonseptic fever and 25 patients with septicemia without endocarditis [3].
• Total PIgA (PIgAT) and PIgA subclass concentrations were measured using a secretory component binding enzyme immunoassay and isotype specific immune complex concentrations were measured using conglutinin (K) binding immunoassays [32].
• They were the radioisotopic conglutinin-binding assay, the Clq-binding assay, and the radial immunodiffusion (RID) of IgG and IgM in PEG precipitates [33].
• Conglutinin microtiter plate ELISA system for detecting circulating immune complexes [34].
• In addition, the presence of abnormal amounts of conglutinin reactive IgA correlated with the recurrence of IgA deposits after renal transplantation (20 patients studied) [35].

References