Specific Host Restance: The Effector Mechanisms
Julius P. Kreier in Infection, Resistance, and Immunity, 2022
This chapter discusses the specific immune effector mechanisms that are responsible for host defense against infection with pathogenic bacteria, viruses, protozoa, and worms. Effector mechanisms mediated directly by antibody will be described first, followed by effector mechanisms mediated by antibody indirectly through the activation of the complement and phagocytic systems. The receptors for the Fc portion of antibody and the receptors for complement products function similarly on macrophages and neutrophils. The classical pathway of complement activation was probably superimposed on the alternative pathway of activation with the result that the functions of the complement system were coordinated with the actions of the antibody system. The first step in activation of complement by the classical pathway is binding of C1 Fc receptors to two or more IgG antibody molecules. The binding of antibody to a microbial surface will cause the deposition and serial activation of complement proteins.
Innate Immunity
Shyamasree Ghosh in Computational Immunology, 2019
This chapter focuses on barriers to infection, pattern recognition receptors (PRRs), chemokines, complement, and cytokines and their function in mediating innate immune responses. Dysregulation or malfunction of the innate immune responses can lead to disease. The innate immune system functions to mediate the destruction of microbes, activation of phagocytosis, and local protective responses called inflammation and trigger tissue repair. The innate immune system cells express a large family of PRRs including Toll-like receptors that can recognise the evolutionarily conserved structures on pathogens called pathogen-associated molecular patterns, which can be proteins, lipids, sugars, nucleic acids, or conjugated moieties of macromolecules. The complement system functions as an integral part of the innate immune response and acts as a bridge between innate and acquired immunity. The innate immune system involves a group of proteins and phagocytic cells that recognise conserved features of pathogens and become quickly activated to help destroy invaders.
1Chapter 1 The Complement System
Julius M. Cruse MD PhD, Robert E. Lewis in Atlas of Immunology, 2010
Throughout the ages man has been fascinated and, at times, obsessed by the marvelous, mysterious, and even baffling qualities of the blood. In 1889, Hans Buchner described a heat-labile bactericidal principle in the blood which was later identified as the complement system. In 1894, Jules Bordet working at the Pasteur Institute in Metchnikoff’s laboratory discovered that the lytic or bactericidal action of freshly drawn blood, which has been destroyed by heating, was promptly restored by the addition of fresh, normal, unheated serum. Paul Ehrlich called Bordet’s alexine “das Komplement.” In 1901, Bordet and Gengou developed the complement fixation test to measure antigen-antibody reactions. Ferrata, in 1907, recognized complement to be a multiple component system, a complex of protein substances of mixed globulin composition present in normal sera of many animal species.
Role of the complement system in NK cell-mediated antitumor T-cell responses
Published in OncoImmunology, 2014
Valérie Janelle, Alain Lamarre
The role of the complement system in oncogenesis and tumor progression remains poorly understood. We have recently demonstrated that the induction of a tumor-specific CD8+ T-cell response is improved upon transient inhibition of the complement system, which is coupled to an increased availability of natural killer cells. The complement system may therefore turn out to constitute a promising target for the development of novel anticancer therapeutics.
Interet Clinique De L’Etude Du Complement
Published in Acta Clinica Belgica, 1976
Summary The complement system is activated via two pathways: the classical pathway which comprises C1, C4 and C2 activation and the alternate pathway in which properdin. C3 and factors B and D are implicated. Complement activation by the classical pathway is induced by Ag-Ab complexes whereas the alternate pathway can be activated by other substances such as polysaccharides. Both pathways lead to the activation of C3 and of the last complement components (C5 to C9). Congenital complement deficiencies affect mainly C1 esterase inhibitors, Clq, Clr, C2, C4, C3, C3b inactivator, C5, C6 and C7. Some of these deficiencies are very well supported by the patient whereas others generate a higher susceptibility to infections, glomerulonephritis and lupus syndromes. Acquired deficiencies of the complement system are always the consequence of other pathological phenomena. Most often they are characterized by a low level of the complement components which are decreased during an activation of the complement system via the classical pathway. In all probability, they are the result of an activation of the complement system by Ag-Ab complexes. Activation of the complement system can be systemic as in SLE, or localized in some extra-vascular fluids such as synovial fluid in the joints of patients suffering from rheumatoid arthritis. In some kidney diseases, the complement profile suggests that there is an activation of the complement system via the alternate pathway.
Avian Antibodies Can Eliminate Interference Due To Complement Activation In ELISA
Published in Upsala Journal of Medical Sciences, 2001
Antibodies derived from egg yolk offer many advantages over mammalian antibodies in several aspects. Chicken antibodies do not activate the human complement system and are sometimes a more suitable choice in designing solid-phase immunometric assays than mammalian antibodies. The material often recommended for immunological assays is serum. A freshly drawn serum sample contains an active complement system, which is inactivated during storage. Mammalian antibodies used in most immunological assays may activate the human complement system. Activated complement components will bind to the antibodies thereby partly block the antibody binding epitopes. We show that an active complement system in undiluted samples reduce the absorbance values by approximately 50 % when using goat antibodies but not when using chicken antibodies. This difference will cause erroneous test results that will vary depending on the handling of the samples. Chicken antibodies can be used to eliminate this interference problem.