About: Complement fixation test is a research topic. Over the lifetime, 4808 publications have been published within this topic receiving 95200 citations. The topic is also known as: complement fixation tests.
TL;DR: The ACIF test was used as a tool to trace the Epstein‐Barr virus genome at the cellular level to study the complementfixing antigens of human lymphoblastoid cell lines.
Abstract: Anti-complement immunofluorescence (ACIF) was used to study the complementfixing antigens of human lymphoblastoid cell lines. These cell lines carry the Epstein-Barr virus (EBV) genome although only producer cultures synthetize EBV-specific antigens (virus capsid antigen, VCA and early antigen, EA) detectable by direct and indirect immunofluorescence, usually in less than 5% of the cells. The ACIF test revealed an antigen localized in the nucleus of the lymphoblastoid cells. In contrast to EA and VCA, this antigen was present in over 90% of the cells of both producer and non-producer cultures. The antigen was shown to be specific for EBV by comparing the reactions of 52 sera in the ACIF test. Sera giving the nuclear reaction contained antibodies to VCA, EA or antigens detectable by complement fixation tests on cell extracts, but sera without EBV antibodies failed to give the reaction. Weak, equivocal or discordant reactions occurred with six sera with low titres in VCA, EA or complement fixation tests. Cell lines derived by transformation of human and primate lymphocytes by EBV gave the nuclear reaction. Control cells with no known association with EBV were non-reactive. These included foetal lymphocytes transformed by phytohaemagglutinin, cell lines derived from breast cancer, glioma, normal glia, pleuritis maligna and myeloma, and two marmoset lymphoid lines carrying Herpesvirus saimiri (HVS). In preliminary experiments, the ACIF test was used as a tool to trace the EBV genome at the cellular level. Cells from two Burkitt lymphoma biopsies, one tested after biopsy and one after passaging in nude mice, contained an EBV-specific antigen. Three clones of cells derived from hybrids of mouse somatic cells and a human lymphoblastoid cell line also contained such an antigen, but the number of reactive cells varied from clone to clone. A fourth clone was non-reactive.
TL;DR: Most qualitative and quantitative antibody tests measure secondary effects of primary antigen-antibody interactions, but they do not always reflect the total antibody content of the antiserum with respect to the test antigen.
Abstract: Most qualitative and quantitative antibody tests measure secondary effects of primary antigen-antibody interactions. Some of these secondary effects are observed in vivo, such as the Arthus phenomenon and anaphylaxis; whereas some are observed in vitro, such as complement fixation, precipitation, erythrocyte agglutination, and hemolysis. These tests measure the capacity of an antiserum to produce the secondary effect selected as the indicator, but they do not always reflect the total antibody content of the antiserum with respect to the test antigen, since antibody in a given antiserum is heterogeneous with respect to the biological or physical effects it produces.1 Examples of diversity of antibody in a single antiserum are numerous even when considering one
TL;DR: Sera of patients with systemic lupus erythematosus were demonstrated to contain precipitating antibodies to soluble tissue components other than DNA, and one dominant reaction was observed which was provisionally termed the Sm system.
Abstract: Sera of patients with systemic lupus erythematosus were demonstrated to contain precipitating antibodies to soluble tissue components other than DNA. One dominant reaction was observed which was provisionally termed the Sm system. The antigen involved was identified in nuclei of a wide variety of cells from different species. It was associated with protein fractions but was a non-histone substance quite sensitive to periodate treatment. Antibodies to the Sm antigen could also be detected by complement fixation. They showed a high incidence in systemic lupus erythematosus with considerable specificity for the disease.
TL;DR: The diagnosis of Q fever relies mainly upon serology, the most commonly used method being the immunofluorescence assay, and serological testing for Q fever should always be done for a patient with a febrile illness and negative blood cultures.
Abstract: My colleagues and I compliment Dr. Fournier and coauthors on an excellent review (3). However, we were surprised to read the statement that there is no commercially available enzyme-linked immunosorbent assay (ELISA) for the serological detection of Q fever, since papers describing these assays have been published (1, 2, 4). These ELISAs, for the detection of specific immunoglobulin M (IgM), IgA, and IgG antibodies produced during Q fever, are available from PanBio Pty Ltd., Brisbane, Australia. All tests use a common assay method, including the provision of cutoff control sera, and take less than an hour to perform. The availability of these tests in part contradicts the claim made by Fournier et al. (3) that ELISA is a more laborious technique than immunofluorescence assay (IFA) and requires considerable experience in interpreting the results. The IgG ELISA has been shown to have good correlation with immunofluorescence, and all patients determined to have a significant level of antibody by IFA were positive in the PanBio test (2, 4). The IgM and IgA ELISAs showed a significant correlation with the complement fixation test, with sensitivity of 100% and specificity of 89% being reported for each assay (1).
TL;DR: Findings show that a rabbit cell surface component can activate the alternate pathway of complement in human serum and suggest that this activation does not involve antibody.
Abstract: The hemolysis of sheep red blood cells (SRBC) occurs via the classical complement pathway and is blocked by ethylene glycol bis-amino tetraacetate (EGTA). By contrast, fresh normal human serum in EGTA buffer was found to cause >90% hemolysis of unsensitized rabbit red blood cells (RaRBC) at a final dilution of 1:15. Absorbing human serum with RaRBC at 0°C will remove only 45% of this hemolytic activity and the same activity is present in human hypogammaglobulinemic serum. When rabbit lymphocytes were incubated with human serum in EGTA buffer, complement fixation occurred on their surface which was demonstrated with radiolabeled antibodies to human C3 or as “blocking” of the complement receptor. With purified complement components it was shown that the EGTA buffer completely blocked C1 but not C4, C2, or the late complement components. These findings show that a rabbit cell surface component can activate the alternate pathway of complement in human serum and suggest that this activation does not involve antibody.