Innate immunity complement system

They activate the complement system (see p. 298) and thereby promote the innate immune defense system (opsonization). 

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. 

Humoral immunity depends on soluble, noncellular effector mechanisms of the immune system. These include defensins and complement components (proteins of the innate immune system) and antibodies (products of the adaptive immune system). They are capable of reacting with foreign substances (e.g., bacteria and viruses) to produce detoxification and elimination. 

Two different systems are involved in the immune response. The innate immune system is based on receptors that can distinguish between bacterial and viral surface structures or foreign proteins (known as antigens) and those that are endogenous. With the help of these receptors, phagocytes bind to the pathogens, absorb them by endocytosis, and break them down. The complement system (see p. 298) is also part of the innate system. 

The complement system is part of the innate immune system (see p. 294). It supports nonspecific defense against microorganisms. The system consists of some 30 different proteins, the "complement factors," which are found in the blood and represent about 4% of all plasma proteins there. When inflammatory reactions occur, the complement factors enter the infected tissue and take effect there. 

The molecular by-products produced by complement activation and by the activities of the innate immune system serve as molecular cues that, in turn, activate the adaptive immune system. 

The complement system is not adaptable and does not change over the course of an individual s lifetime as such it belongs to the innate immune system. However, it can be recruited and... 

As stated above, the principal objective for the use of an adjuvant in a vaccine is to potentiate immune response to an Ag of minimal immunogenicity. How this potentiation is achieved varies from adjuvant to adjuvant and in many cases, the precise mechanism of ac tion is unknov n. However, as a rule, immune potentiation is accomplished by the ability of the adjuvant to induce a variety of non-specific activities within the innate arm of the immune system. Once activated, the innate branch of immunity, particularly the complement system, orchestrates the various humoral and cell-mediated responses that operate within and between the innate and acquired arms. The result is a generalized activation and potentiation of the immune system in response to the adjuvant with the hope that this generalized immune priming will allow for a more effective processing and recognition of the Ag contained within the vaccine. 

As described above, traditional adjuvants typically are derived from bacterial components in order to provide the bacteria signals necessary for the activation and potentiation of the innate arm of the immune system. One of the first components of innate immunity that becomes ac tivated in response to these bacterial signals is the complement system. 

CRP content indicates a persistent proinflammatory stimulus in the body. CRP binds to host or bacterial phosphocholine, and the complex activates a group of plasma proteins called complement (Sect. 3.3.2). The complement system resembles the blood clotting system, except that proteolytic cleavage of its components results in peptide fragments that to attract and enhance the phagocytosis (opsonization) of CRP- or antibody-bound material by macrophages (like IL-1 or IL-8). CRP is part of the innate immune response, and the antibody response is part of the acquired immune response (Sect. 12.1.4). Many bacteria of the successor microbiota induce an antibody response that is increased in periodontitis compared with gingivitis or healthy subjects. 

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