C1q Antibodies Research Articles

Glomerular deposition of C1q and anti-C1q antibodies in mice following injection of antimouse C1q antibodies.

Anti-C1q autoantibodies are present in the serum of patients with different autoimmune diseases such as systemic lupus erythematosus (SLE). The occurrence of these autoantibodies correlates with renal involvement. In the present study we examined whether injection of rabbit antimouse C1q antibodies in mice leads to deposition in kidneys. Injection of healthy mice with a single dose of rabbit IgG antimouse C1q antibodies resulted in deposition of both C1q and IgG anti-C1q in glomeruli. The pattern of deposition observed in the glomeruli of mice injected with antimouse C1q antibodies both at 24 h and 2 weeks was both glomerular basement membrane (GBM)-associated and mesangial. Injection of control IgG did not have a detectable effect on circulating C1q levels, and no deposition of either C1q or rabbit IgG was seen at 24 h. The deposition of rabbit antimouse C1q and C1q in glomeruli resulted in complement activation, as assessed by C3 deposition, and influx of leucocytes associated with albuminuria in some, but not all mice. In none of the control mice was albuminuria observed. This report is the first to show that anti-C1q antibodies deposit in the healthy glomerulus together with autologous C1q. This deposition is stable for at least 2 weeks, causes complement activation, leucocyte influx and can lead to mild albuminuria.

Role of C1q and C1q receptors in the pathogenesis of systemic lupus erythematosus.

The association between C1q and autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus (SLE) is well established. Deficiency in C1q is considered to be a strong susceptibility factor and is corroborated by the fact that > or = 92% of the known cases of hereditary deficiency in C1q develop rheumatic disease. Furthermore, the observation of the presence of high-affinity autoantibodies against C1q antibodies in patients with SLE provides a strong correlation between these antibodies and the inflammatory processes that occur in this disease. Recent evidence using C1q-deficient mice has shown the presence of glomerulonephritis with immune deposits and a large number of apoptotic bodies in the diseased glomeruli suggesting a defect in the clearance of apoptotic cell by macrophages and dendritic cells (DCs). Although these data are consistent with the hypothesis that C1q deficiency may induce a generalized failure to clear immune complexes and apoptotic cells, this concept alone cannot wholly explain why individuals with C1q deficiency are prone to develop SLE. Therefore, C1q alone or in conjunction with other surface molecules must play a much more fundamental role in immunoregulation, especially those processes that regulate T cell function and tolerance. In support of this hypothesis is the finding that C1q causes inhibition of mitrogen-induced T cell-proliferative response by interaction with C1q receptors. Furthermore, macrophages and possibly DCs not only synthesize but also display C1q as a type II cell surface molecule, especially at sites of inflammation. Although it is not yet known what role the surface-expressed C1q plays, it is tempting to assume that it plays a role in the priming of naïve T cells by DCs. This work will review the current concepts of the role of C1q and C1q receptors in autoimmunity.

Mesangial deposition of IgA2 subclass and lectin pathway‐mediated complement activation in IgA glomerulonephritis

Three pathways are recognized in the complement activation cascade. The aim of our study was to elucidate immunohistologically which complement pathway is associated with the activation in IgA glomerulonephritis (GN) and the relation of IgA subclass to the complement activation. Immunohistological staining was performed on biopsied renal specimens from 36 patients with IgA GN, 10 with systemic lupus erythematosus (SLE) and 16 with other glomerulonephritides using polyclonal antibodies of IgG, IgA, IgM, C3c, C4, C1q and monoclonal antibodies of IgA1, IgA2, mannose‐binding lectin (MBL) and MBL‐associated serine protease‐1 (MASP‐1). Mesangial deposits of IgA1, IgA2, C3c, C4, MBL and MASP‐1 were detected in 19 of the 36 patients with IgA GN, and IgA2 and MBL/MASP‐1 were colocalized in the mesangium in these 19 patients. The remaining 17 patients showed mesangial deposition of IgA1 alone. Twelve of these 17 patients presented mesangial deposition of C3c without deposition of C4, MBL and MASP‐1. No deposition of C1q was evident in IgA GN patients. Three of the 10 SLE patients showed glomerular deposition of MBL and MASP‐1 without deposition of IgA2. No patient with other glomerulonephritides showed glomerular deposition of IgA1, IgA2, MBL and MASP‐1. There was no correlation in clinical and pathological indicators between IgA2‐positive and IgA2‐negative patients with IgA GN. In conclusion, alternative pathway‐mediated complement activation is associated in patients with mesangial deposition of IgA1 alone in IgA GN. In those with the deposition of both IgA1 and IgA2, both alternative and lectin pathways are activated, and mesangial deposition of IgA2 is associated with the lectin pathway‐mediated complement activation in IgA GN.

Mesangial IgA2 deposits and lectin pathway-mediated complement activation in IgA glomerulonephritis

Three pathways are recognized in complement activation. The aim of our study is to elucidate immunohistologically which complement pathway is associated with complement activation in immunoglobulin A (IgA) glomerulonephritis (GN) and which IgA subclass is related to complement activation. Immunohistological staining was performed on renal biopsy specimens obtained from 36 patients with IgA GN, 10 patients with systemic lupus erythematosus (SLE), and 16 patients with other GNs using polyclonal antibodies of IgG, IgA, IgM, C1q, C3c, and C4 and monoclonal antibodies of IgA1, IgA2, mannose-binding lectin (MBL), and MBL-associated serine protease-1 (MASP-1). Mesangial deposits of both IgA1 and IgA2 were found in 19 of 36 patients with IgA GN. Mesangial deposits of C3c, C4, MBL, and MASP-1 also were detected in these 19 patients, and IgA2, MBL, and MASP-1 deposits were colocalized in the mesangium in these patients. The remaining 17 patients showed mesangial deposits of IgA1 alone. Twelve of these 17 patients showed mesangial deposits of C3c without C4, MBL, or MASP-1. No deposition of C1q was evident in patients with IgA GN. Three of 10 patients with SLE showed glomerular deposition of MBL and MASP-1 without glomerular deposition of IgA2. None of the patients with other GNs showed glomerular deposition of IgA1, IgA2, MBL, or MASP-1. There was no correlation in clinical or pathological indicators between IgA2-positive and IgA2-negative patients with IgA GN. In conclusion, alternative pathway-involved complement activation is associated with mesangial deposits of IgA1 alone in patients with IgA GN. In those with mesangial deposits of both IgA1 and IgA2, both the alternative and lectin pathways are involved in complement activation. We first report that mesangial deposits of IgA2 may activate the lectin pathway in patients with IgA GN. © 2001 by the National Kidney Foundation, Inc.

Correlation of the Expression Level of C1q mRNA and the Number of C1q-Positive Plaques in the Alzheimer Disease Temporal Cortex

We compared the expression level of C1q mRNA and the number of C1q-positive plaques in adjacent or nearby brain sections from Alzheimer disease (AD) and control cases. Small blocks of temporal cortex were fixed with 4% paraformaldehyde for 2 days at 4°C. After cryoprotection with solutions containing 10–20% glycerol and 2% dimethylsulfoxide, 40-µm sections were cut from the tissue blocks. A section from each case was stained by immunohistochemistry using a C1q antibody, while RNA was purified from adjacent or nearby sections using a combination of proteinase K pretreatment followed by extraction using Trizol reagent. The expression of C1q B chain mRNA was analyzed in these samples by the reverse-transcription polymerase chain reaction (RT-PCR). The intensities of the PCR products were measured by an image analyzer. The expression of C1q B chain mRNA was significantly more abundant in AD than in control cases (p < 0.05). Immunohistochemical analysis showed that C1q protein was localized in senile plaques in the AD brain. The number of C1q-positive plaques correlated with the expression level of C1q gene (p < 0.05). The present results suggest that C1q protein in senile plaques originates is endogenously produced in the AD brain.

Recombinant adenovirus gene transfer in adults with partial ornithine transcarbamylase deficiency (OTCD).

Human Gene TherapyVol. 10, No. 14 Recombinant Adenovirus Gene Transfer in Adults with Partial Ornithine Transcarbamylase Deficiency (OTCD)Mark L. Batshaw, James M. Wilson, Steven Raper, Marc Yudkoff, and Michael B. RobinsonMark L. BatshawSearch for more papers by this author, James M. WilsonSearch for more papers by this author, Steven RaperSearch for more papers by this author, Marc YudkoffSearch for more papers by this author, and Michael B. RobinsonSearch for more papers by this authorPublished Online:6 Jul 2004https://doi.org/10.1089/10430349950017068AboutSectionsPDF/EPUB ToolsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail FiguresReferencesRelatedDetailsCited byAbnormalities of Hepatic Protein MetabolismAdenoviral Vector-Based Vaccines and Gene Therapies: Current Status and Future Prospects13 March 2019Spliced: Boundary-work and the establishment of human gene therapy28 June 2017 | BioSocieties, Vol. 12, No. 2Adenoviruses7 March 2016The Ethics of Randomized Trials in Oncology25 November 2014Turning the Corner with Viral-based Gene Therapy—Development of the Rogue BiopharmaceuticalGene TherapyVirus-mediated gene delivery for human gene therapyJournal of Controlled Release, Vol. 161, No. 2Radioprotective gene therapy2 May 2011 | Expert Opinion on Biological Therapy, Vol. 11, No. 9The Death of Jesse Gelsinger: New Evidence of the Influence of Money and Prestige in Human Research1 June 2010 | American Journal of Law & Medicine, Vol. 36, No. 2-3Complement Component C1q and Anti-hexon Antibody Mediate Adenovirus Infection of a CAR-Negative Cell Line Van Tsai, Robin Varghese, Sundari Ravindran, Robert Ralston, and Gary Vellekamp30 December 2008 | Viral Immunology, Vol. 21, No. 4The gene delivery system for rheumatoid synoviumJapanese Journal of Clinical Immunology, Vol. 31, No. 1Gene therapy. An ethical profile of a new medical territory1 January 2006 | The Journal of Gene Medicine, Vol. 8, No. 11Replication Properties of Human Adenovirus In Vivo and in Cultures of Primary Cells from Different Animal SpeciesJournal of Virology, Vol. 80, No. 7CANCER GENE THERAPY CLINICAL TRIALSGene therapy for hemophilia?9 June 2005 | Journal of Thrombosis and Haemostasis, Vol. 3, No. 6Regulatory Aspects in the Development of Gene TherapiesGene therapy for genetic diseases: On the horizonClinical and Applied Immunology Reviews, Vol. 4, No. 6Endocrine Aspects of Cancer Gene Therapy31 October 2016 | Endocrine Reviews, Vol. 25, No. 1Metabolic and neuropsychological phenotype in women heterozygous for ornithine transcarbamylase deficiency1 January 2003 | Annals of Neurology, Vol. 55, No. 1Not so rare: errors of metabolism during the neonatal periodNewborn and Infant Nursing Reviews, Vol. 3, No. 4Gene Therapy Applications for Spine FusionSpine, Vol. 28, No. supplementTiter determination of Ad5 in blood: a cautionary note30 May 2003 | Gene Therapy, Vol. 10, No. 12The impact of adenovirus infection on the immunocompromised host1 January 2003 | Reviews in Medical Virology, Vol. 13, No. 3Ornithine transcarbamylase deficiency: a urea cycle defectEuropean Journal of Paediatric Neurology, Vol. 7, No. 3Gene therapy ethics and haemophilia: an inevitable therapeutic future?4 March 2003 | Haemophilia, Vol. 9, No. 2Adenoviral vectors: Systemic delivery and tumor targeting22 November 2002 | Cancer Gene Therapy, Vol. 9, No. 12Novel, Chimpanzee Serotype 68-Based Adenoviral Vaccine Carrier for Induction of Antibodies to a Transgene ProductJournal of Virology, Vol. 76, No. 6Subcutaneous Administration of a Replication-Competent Adenovirus Expressing HSV-tk to Cotton Rats: Dissemination, Persistence, Shedding, and Pathogenicity Oliver Wildner and John C. Morris6 July 2004 | Human Gene Therapy, Vol. 13, No. 1Lethal Toxicity, Severe Endothelial Injury, and a Threshold Effect with High Doses of an Adenoviral Vector in Baboons Núria Morral, Wanda K. O'Neal, Karen Rice, M. Michelle Leland, Pedro A. Piedra, Estuardo Aguilar-Córdova, K. Dee Carey, Arthur L. Beaudet, and Claire Langston6 July 2004 | Human Gene Therapy, Vol. 13, No. 1Quantitative Analysis of Adenovirus-Specific CD4+ T-Cell Responses from Healthy Adults Melanie Olive, Laurence C. Eisenlohr, and Phyllis Flomenberg9 July 2004 | Viral Immunology, Vol. 14, No. 4Complement activation by recombinant adenoviruses24 January 2002 | Gene Therapy, Vol. 8, No. 23Adenovirus Type 7 Induces Interleukin-8 Production via Activation of Extracellular Regulated Kinase 1/2Journal of Virology, Vol. 75, No. 14Update on adenovirus and its vectorsJournal of General Virology, Vol. 81, No. 11Adenovirus-mediated gene therapy to liver grafts: Successful gene transfer by donor pretreatmentSurgery, Vol. 128, No. 2Viral Vectors for Gene TransferDrugs, Vol. 60, No. 2Altering the pathway to human gene therapy24 December 2001 | Clinical Genetics, Vol. 58, No. 1Latest Developments in Gene Transfer Technology: Achievements, Perspectives, and Controversies over Therapeutic Applications1 January 2009 | STEM CELLS, Vol. 18, No. 1 Volume 10Issue 14Sep 1999 To cite this article:Mark L. Batshaw, James M. Wilson, Steven Raper, Marc Yudkoff, and Michael B. Robinson.Recombinant Adenovirus Gene Transfer in Adults with Partial Ornithine Transcarbamylase Deficiency (OTCD).Human Gene Therapy.Sep 1999.2419-2437.http://doi.org/10.1089/10430349950017068Published in Volume: 10 Issue 14: July 6, 2004PDF download

C1q autoantibodies in HIV infection: correlation to elevated levels of autoantibodies against 60-kDa heat-shock proteins.

Antibodies to solid phase C1q (C1qAb) were determined in 295 serum samples from 132 HIV-infected subjects and in sera from 140 HIV-seronegative healthy individuals as control. An ELISA method applied for the determination of C1qAb in other diseases was used. In part of these sera, other autoantibodies (antibodies reacting with 60-kDa human heat shock protein (hsp60) or mycobacterial hsp65; IgA and IgG class antibodies against the Fab and F(ab')2 moieties of IgG) as well as complement-mediated antibody-dependent enhancement/neutralization (C'-ADE) were also determined. Increased amount of C1qAb was found in HIV-infected subjects as compared with HIV-seronegative controls (P = 0.0138). In 17 of 132 (13.0%) seropositive individuals but only in 7/140 (5.0%) samples from the controls, the amount of C1qAb exceeded the upper limit (95th percentile) of the normal values (P = 0.031). The amount of C1qAb significantly decreased during a follow-up period of 65 months. C1qAb levels were found to strongly correlate to hsp60/65 autoantibodies but did not correlate or only weakly correlated to the amount of anti-Fab or anti-F(ab')2 autoantibodies measured in the same serum samples. Anti-C1q antibodies recognized the solid phase hsp60/65. Three predicted epitope regions of M. paratuberculosis hsp65 were able to bind efficiently C1q antibodies. An inverse correlation was found between C1qAb and C'-ADE, neutralization was more frequent in the sera with detectable C1qAb, whereas sera without C1qAb more likely enhanced HIV infection in vitro.

C1q as Antigen in Hurnoral Autoirnmune Responses

The observation of anti-C1q antibodies (C1qAb) in patients with various autoimmune diseases has led to the establishment of a strong correlation between these antibodies and renal involvement in patients with systemic lupus erythematosus (SLE). The measurement of anti C1q antibodies requires detailed insight in the reactivity of C 1q with immune complexes and the methods to detect C1q as an antigen by solidphase assays. In this overview we describe the pitfulls of the anti C1qAb assay and its use in the measurement of C1qAb. Further we discuss the relevance of C1gAb in the pathogenesis of SLE and especially in relation to lupus nephritis.

Both IgG- and C1q-receptors play a role in the enhanced binding of IgG complexes to human mesangial cells.

The presence of immunoglobulin G (IgG) in the mesangial area in kidneys of patients with different forms of glomerulonephritis suggests a role for IgG in the inflammatory process. This study investigates whether IgG is able to bind to cultured human mesangial cells (MC) in vitro. Incubation of MC with 125I-aggregated IgG(125I-AIgG), as a model for immune complexes (IC), at 4 degrees C resulted in a time- and dose-dependent binding of 125I-AIgG to MC. The binding of 125I-AIgG to MC was inhibited by excess AIgG or Fc-fragments and not by F(ab')2-fragments or human serum albumin (HSA). Scatchard analysis revealed the presence of 2.8.10(6) receptors/cell with an affinity of 9.7.10(7) M-1. Incubation of MC with 125I-C1q resulted in a time- and dose-dependent binding of 125I-C1q to MC. The binding of 125I-C1q was inhibited by excess C1q or C1q talls and not by HSA. Scatchard analysis revealed the presence of 3.2.10(7) binding sites/cell with an affinity of 1.4.10(7) M-1. Immunoprecipitation of 125I-labeled MC membrane proteins with C1q or monoclonal antibodies directed against human C1q-R revealed a single 66 to 68 kd band under reducing conditions. Fluorescence-activated cell-sorter analysis revealed an average of 60.1% +/- 5.4% of the cells positive with a mean channel of fluorescence of 592. A cooperative effect between C1q-R and Fc gamma-R in the binding of 125I-AIgG to MC, was assessed by incubation of 125I-AIgG in the presence of increasing concentrations of C1q, C1q talls, or delta C1q. Only intact C1q showed a 6- to 11-fold enhancement in binding of 125I-AIgG to MC. These studies demonstrate the occurrence of C1q-R and Fc gamma-R on MC and indicate that binding of IC is enhanced after interaction of IC with C1q.

Binding of surfactant protein A to C1q receptors mediates phagocytosis of Staphylococcus aureus by monocytes

During both steady-state conditions and inflammatory reactions in the lower airways, monocytes migrate to the alveoli where they come into contact with surfactant. Surfactant is composed of phospholipids, neutral lipids, and specific proteins, and its main function is to reduce surface tension in the alveoli. The most abundant glycoprotein surfactant protein A (SP-A) affects the structure, function, and metabolism of pulmonary surfactant. The aim of the present study was to determine whether SP-A plays a role in the antibacterial activities of human monocytes and whether this is mediated by a receptor for SP-A on these cells. The results showed that SP-A binds to both Staphylococcus aureus and monocytes and mediates the phagocytosis of the bacteria by these cells. SP-A does not stimulate the intracellular killing of bacteria by monocytes, and SP-A-opsonized S. aureus do not induce the production of reactive oxygen intermediates. SP-A binds to the C1q receptor (C1qR) on monocytes, since its binding was inhibited by C1q and the SP-A-enhanced association of S. aureus with these cells was completely abolished when monocytes were adherent to surfaces coated with C1q or anti-C1qR monoclonal antibody. Furthermore, the binding of SP-A to monocytes results in an increased intracellular concentration of adenosine 3',5'-cyclic monophosphate. Together, these results demonstrate that C1qR mediates the phagocytosis of SP-A-opsonized S. aureus by monocytes.

Platelet activation and inhibition of malarial cytoadherence by the anti-CD36 IgM monoclonal antibody NL07

The surface glycoprotein CD36 (GPIV) is known to mediate the adhesion of Plasmodium falciparum malaria-infected red blood cells and to be a receptor for extracellular matrix proteins such as collagen and thrombospondin. The murine monoclonal IgM antibody NL07, which is specific for CD36, has now been shown to also be a potent inhibitor of the adhesion of P falciparum malaria-infected red blood cells to C32 melanoma cells. Treatment of platelets with NL07 monoclonal antibody resulted in rapid degranulation, release of ATP and serotonin, increase in [Ca2+]i, and tyrosine phosphorylation of a substrate protein of 130 kD. In about one-half of the experiments, activation with NL07 resulted in the formation of small aggregates of 10 to 30 platelets, whereas in the other half of the experiments, large aggregates were seen similar to those induced by adenosine diphosphate (ADP) and these large aggregates could be converted to the small aggregates by ATP alpha S or by AP-2 or other antibodies against GPIIb and/or IIIa. Microaggregates of 2 to 5 platelets were seen with Glanzmann's platelets that constitutively lack GPIIb/IIIa. Aggregate formation was not seen with heat-treated serum, in the presence of anti C1q antibodies, or when using C5-, C8-, or C9-deficient human sera. Although activation of platelets with purified complement components results in a slow morphologic change without aggregation, involvement of CD36 results in rapid complement-mediated activation leading to formation of small aggregates that is largely independent of GPIIb/IIIa and that, under certain circumstances, proceeds to the formation of large ADP-dependent aggregates.

Expression and function of gingival fibroblast C1q receptors are upregulated by interleukin‐1β and transforming growth factor‐β

In injury and inflammation, complement (C) component C1q, in addition to its central role in initiation of classical pathway of complement activation, modulates diverse cellular functions by binding to specific cell surface receptors. Interaction of substrate-bound C1q with receptors for the collagen-like domain of C1q (C1qRC) of human gingival fibroblasts (HGF) promotes cell attachment. We investigated modulation of the adhesive function and expression of C1qRC by interleukin-1 beta (IL-1 beta) and transforming growth factor-beta (TGF-beta). Confluent fibroblast monolayers were incubated under standard culture conditions with or without cytokines. C1qRC function was measured by attachment assays. IL-1 beta and TGF-beta increased fibroblast adhesion to C1q to 146% and 131% of controls, respectively. Cytokine enhancement of HGF adhesion was concentration-dependent, saturable (20 ng/ml IL-1 beta; 1 ng/ml TGF-beta) and time-dependent (IL-1 beta 12-hr peak; TGF-beta 24-hr peak). Effect of IL-1 beta and TGF-beta on C1qRC expression was assessed by flow cytometry measurements of fluorescence intensity of cells stained with C1q and FITC anti-C1q antibody, and by binding studies with 125I-C1q. Cells treated with cytokines displayed a two- to four-fold increased fluorescence of cell-bound C1q compared to controls. Binding studies indicated the increased fluorescence correlated with increase in number of C1qRC in both IL-1 beta (4.7 x 10(6)/cell) and TGF-beta (3.9 x 10(6)/cell)-treated cells, compared to control (3.0 x 10(6)/cell), but had no effect on binding affinity. Rates of internalization of receptor-bound C1q were similar in cytokine-treated cells and controls. We propose from these data that IL-1 beta and TGF-beta have the ability to upregulate C1qRC expression, and this effect contributes to increased adhesion of HGF to substrate-bound C1q.

High Doses of Intravenous Immunoglobulin Do Not Affect the Recognition Phase of the Classical Complement Pathway

We have recently found that intravenous immunoglobulin (IVIg) prevents deposition of C3 and C4 fragments onto antibody sensitized erythrocytes. To find out if such an effect results from the blockade of the recognition phase of the classical complement cascade, we investigated the ability of human serum containing high concentrations of IVIg to deposit the recognition subunit of the first complement component (C1q) onto targets. Normal human serum supplemented in vitro with IVIg did not demonstrate reduced C1q binding to targets as determined by radiolabeled antihuman C1q antibody uptake. Similarly, methylamine-treated normal human serum to which IVIg was added was equally effective in terms of C1q binding as the same serum without IVIg. At increasing doses of sensitizing antibody, C1q uptake decreased proportionally; however, at all antibody dilution points C1q uptake was not significantly different in the serum with IVIg in comparison with normal serum. Serum from a patient treated with IVIg did not differ in its capacity to deposit C1q from the same patient's serum before therapy. Our data suggest that IVIg does not interfere with the recognition step of classical complement pathway. This is a US government work. There are no restrictions on its use.

High doses of intravenous immunoglobulin do not affect the recognition phase of the classical complement pathway

We have recently found that intravenous immunoglobulin (IVIg) prevents deposition of C3 and C4 fragments onto antibody sensitized erythrocytes. To find out if such an effect results from the blockade of the recognition phase of the classical complement cascade, we investigated the ability of human serum containing high concentrations of IVIg to deposit the recognition subunit of the first complement component (C1q) onto targets. Normal human serum supplemented in vitro with IVIg did not demonstrate reduced C1q binding to targets as determined by radiolabeled antihuman C1q antibody uptake. Similarly, methylamine-treated normal human serum to which IVIg was added was equally effective in terms of C1q binding as the same serum without IVIg. At increasing doses of sensitizing antibody, C1q uptake decreased proportionally; however, at all antibody dilution points C1q uptake was not significantly different in the serum with IVIg in comparison with normal serum. Serum from a patient treated with IVIg did not differ in its capacity to deposit C1q from the same patient's serum before therapy. Our data suggest that IVIg does not interfere with the recognition step of classical complement pathway. This is a US government work. There are no restrictions on its use.

Solid phase indirect radioimmunoassays for the rapid diagnosis of Sindbis virus antigen.

Indirect radioimmunoassays have been developed for the rapid detection of Sindbis virus. Dilutions of Sindbis virus from tissue culture fluids have been immobilized and allowed to react with rabbit anti-Sindbis virus antibodies. The bound antibodies were assayed either by 125I-labelled anti-rabbit IgG-antibodies or alternatively by addition of human complement and 125I-labelled anti-human C1q antibodies or 125I-labelled protein A.