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Specific Host Restance: The Effector Mechanisms
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
While the entire process is very complex in its details, the basic principles are few: in the classical pathway complement fixation is triggered by antibody binding to antigen; complement proteins are activated by proteolysis; some fragments become active proteases, furthering and amplifying the entire process, and others become soluble molecules that play other roles in the immune response. The final step is the production of a macromolecular complex that forms a hole in the membrane and destroys the microbe.
Infection and immunology
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
Although cold agglutinins are increased in Mycoplasma pneumoniae infections, they are not diagnostic and have been found in association with other viral respiratory infections. M. pneumoniae may cause pneumonia in any age group but it most commonly affects adolescents and young adults. It may cause upper respiratory disease and has been isolated from patients with otitis media. The organism cannot be isolated easily from the sputum. Complement fixation is the best serological test for the diagnosis. The organism is sensitive to erythromycin and tetracycline.
Immunological Approaches
Published in Adorjan Aszalos, Modern Analysis of Antibiotics, 2020
Deborah E. Dixon, Susan J. Steiner, Stanley E. Katz
The complement fixation assay is based upon the phenomenon of immune hemolysis. The assay is performed in two stages. In stage 1, the antibody and the antigen are mixed in equivalent amounts in the presence of carefully measured amounts of complement. If one of these, either antibody or antigen, is lacking, there will be no fixation of complement. In stage 2, if the antibody-antigen complexes are formed and complement is fixed, hemolysis will not occur. If hemolysis does occur, complement remains and an effective antibody-antigen reaction did not occur. Hence, hemolysis or the degree thereof becomes the end point measurement.
An overview of advancement in aptasensors for influenza detection
Published in Expert Review of Molecular Diagnostics, 2022
Varsha Gautam, Ramesh Kumar, Vinod Kumar Jain, Suman Nagpal
Although there are many identification strategies available today, such as rapid influenza diagnostic tests (RIDTs). Enzyme linked immunosorbent assay (ELISA). Double immunodiffusion (DID). Complement fixation test (CF). Hemagglutinin inhibition (HI). Nucleic acid-based assays (NATs), and real time polymerase chain reaction (RT-PCR), but their specificity and time effectiveness still make them less applicable. The flu virus is a ‘form shifter.’ and new plans have to be drawn periodically to improve the vaccine for that year’s influenza outbreak. It has been challenging because of the variability of the influenza strain. Therefore, early identification is the only key available. Present viral diagnosis relies on viral nucleic acid or protein components being selectively identified. Because of specialized laboratory requirements, culture methods can be excluded. Additionally, serological testing is ineffective, requires two sufficient specimens, and takes time. Rapid tests can only detect nucleic acids or a few viral antigens and encourage practical and informative diagnosis. Moreover, RT-PCR is still regarded as costly and time consuming, and ELISA testing does not offer a high degree of sensitivity [14].
Managing complications secondary to Waldenström’s macroglobulinemia
Published in Expert Review of Hematology, 2021
Ilias Pessach, Meletios A. Dimopoulos, Efstathios Kastritis
In approximately 10% of WM patients, the monoclonal IgM may behave as a cold-reactive antibody that recognizes erythrocyte antigens at normal body temperatures and displays progressively greater affinity for the erythrocytes at lower temperatures. As a result, patients with cold agglutinin activity may present with acrocyanosis, Raynaud’s syndrome, or of moderate severity chronic hemolytic anemia [52]. Most patients with cold agglutinin activity present with a chronic stable anemia that does not require active therapy beyond folate and iron supplementation. However, in patients with symptomatic anemia, treatment should aim in reducing the production of the IgM monoclonal protein responsible for complement fixation on the red blood cells. In these patients, BR combination is highly efficient and safe, inducing durable responses and could be considered as first-line therapy; other combinations containing PIs may also be active [45,53]. Experience with ibrutinib is limited, but available data indicate safety and efficacy [54]. In frail patients, rituximab monotherapy could be considered but responses are usually not durable (less than a year) and there is a risk of IgM flare-related exacerbation of hemolysis [52]. In rare cases PLEX could also be an option for short-term immediate IgM reduction.
Preclinical characterization of dostarlimab, a therapeutic anti-PD-1 antibody with potent activity to enhance immune function in in vitro cellular assays and in vivo animal models
Published in mAbs, 2021
Sujatha Kumar, Srimoyee Ghosh, Geeta Sharma, Zebin Wang, Marilyn R. Kehry, Margaret H. Marino, Tamlyn Y. Neben, Sharon Lu, Shouqi Luo, Simon Roberts, Sridhar Ramaswamy, Hadi Danaee, David Jenkins
To assess the potential for complement fixation by dostarlimab, an ELISA-based C1q binding assay was employed. Dostarlimab or a positive control (MabThera) was coated onto a 96-well polystyrene plate at 8 concentrations: 10, 7.7, 5.9, 4.6, 3.5, 2.7, 2.1, and 1.6 µg/mL. The plate was incubated overnight (2–8°C) and then aspirated. The plate was blocked for 1 hour at room temperature with 1X PBS supplemented with 0.3% BSA and 0.05% Tween 20 before being washed with 10 mM phosphate buffer at pH 7.4 supplemented with 140 mM NaCl, 2.7 mM potassium chloride, and 0.05% Tween 20. Recombinant human C1q (10 µg/mL; Quidel) was added to each well and incubated for 2 hours at room temperature. After incubation, the plate was washed and a sheep anti-human C1q/horseradish peroxidase conjugate (0.5 µg/mL; Abcam, Cat#ab46191) added. The plate was incubated for 1 hour at room temperature, washed, and SuperSignal ELISA Femto Substrate (1:1 mixture of luminol/enhancer and stable peroxide solution; Thermo Fisher Scientific) added to all wells. The plate was read within 1–5 minutes on a luminometer (MS SpectraMax), measuring total light output in relative light units (RLU). Four parameter nonlinear regression analyses were performed on each antibody titration, and EC50 values were calculated.