Proteins complement system

A cascade of proteins of the immune response that can be triggered by antigen-antibody complexes and by the innate immune system (e.g. exposure to microbial polysaccharides) to raise the immune response. Complement proteins can detect and bind to foreign material or immune complexes and label them for phagocytosis. They can also cause inflammation by directly degranulating mast cells and releasing chemokines to recruit other immune cells into the affected area. 

An example that alterations in the ubiquitin-proteasome system may be a primary event in AD, after ABP-induced toxicity or accumulation, was provided by Konishi et al. (273), who found that frameshift ubiquitin-B was present in subjects with AD pathology prior to development of dementia, probably accumulating in the initial steps of AD pathogenesis, whereas complement proteins were detected in AD patients but not in subjects with AD pathology and no symptoms of dementia, indicating the involvement of complement proteins in the later stage of dementia (273). 

Lissauer, M.E., et al. (2007) Coagulation and complement protein differences between septic and uninfected systemic inflammatory response syndrome patients. / Tmuma. 62, 1082-92 discussion 1092-4. 

Biochemical (at the molecular level) defense systems (e.g., complement proteins)... 

The C-terminal domain is a Ca2+-dependent C-type lectin (Chapter 4), while the N-terminal domain is involved in oligomer formation through disulfide bridges. The overall structure is similar to that of the complement protein Clq (Chapter 31).e) Protein D is also collagen-like1 but evidently plays a very different functional role than SP-A. The latter associates with the major surfactant lipids but SP-D does not. It does bind phosphatidyl inositol" and gluco-sylceramide, lipids that are present in small amounts. Perhaps SP-D helps to remove these polar lipids which might interfere with surfactant action.6 Both proteins A and D may also have functions in the immune system.1... 

Both C3b and C4b bind tightly to cell surfaces, a feature that helps to direct the complement system s attack to the surfaces of invading organisms. This tight binding also involves covalent attachment of macromolecules by reaction with a preformed thioester just as with a2-macroglobulin.hd In fact, the thioester linkage was first discovered in the complement proteins. Both C3 and C4 contain the thioester... 

The activation, maturation, differentiation, and mobilization of immune cells are controlled by cytokines (e.g., interleukins, interferons, and chemokines), which are soluble mediators produced by immune cells and/or by cells outside the immune system (e.g., epithelial cells and cells of the nervous system). Other soluble (humoral) mediators produced by immune cells include antibodies (immunoglobulins) and complement proteins (plasma proteins produced by monocytes and macrophages as well as hepatocytes). Mediators are important in the implementation and regulation of immune responses. 

Before the characterization of chemokines the largest protein chemoattractant known was complement factor 5a. Complement protein 5 is proteolytically processed by the complement system during inflammation. 

Inflammation is a local protective response to infection or injury whereby cells and proteins in the blood enter to remove the pathogens and repair the damaged tissue. Edema, redness, pain, and heat are the four cardinal symptoms of inflammation. Extent of reactions is determined by inflammatory mechanisms mediated by serum protein or cellular systems. Serum protein systems include complement, coagulation, fibrinolysis, and kinin cellular systems include PMN cells, mast cells, platelets, eosinophils, lymphocytes, macrophages, and reticuloendothelial system. Insufficient responses result in immunodeficiency leading to cancer and infections excessive responses are the cause of a number of chronic diseases like diabetes, cardiovascular disease, rheumatoid arthritis, multiple sclerosis, and Alzheimer s disease (Tracey, 2002). 

Morita H, Suzuki K, Mori N, Yasuhara O. Occurrence of complement protein C3 in dying pyramidal neurons in rat hippocampus after systemic administration of kainic acid. Neurosci Lett 2006 409 35 0. 

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