Understanding Nonspecific Immune Defense Mechanisms

Nonspecific Immune Defense Mechanisms

Nonspecific mechanisms include the inflammatory response, activation of the complement system, and the action of interferon. These mechanisms are highly effective, and few foreign elements bypass this control. However, when a pathogen escapes, specific mechanisms are activated, namely the cellular immune response and the humoral immune response.

The Inflammatory Response

This mechanism activates when the skin or mucous membranes are injured. The symptoms of inflammation are easily recognizable:

• Redness
• Swelling
• Local pain
• Fever

Why do these symptoms occur? The redness of a wound is caused by an increase in blood flow to the area. This increase is due to the release of pyrogenic substances, such as histamine, by damaged cells. By increasing blood flow, the volume of the zone increases, resulting in tissue swelling and pressure on nerve endings, which causes pain. Fever is also a consequence of local pyrogenic agents; the elevated temperature activates the metabolism of macrophages and inhibits bacterial division.

The Complement System

The complement system consists of 21 plasma proteins synthesized by the liver and locally by macrophages. The mechanism of action occurs via an activation cascade, where each step of the reaction process is amplified because each enzyme can activate several molecules, which in turn activate others. The activation involves the breakdown (proteolysis) of inactive proteins into several fragments that act on the next protein. There are two mechanisms of activation: the alternative pathway and the classical pathway.

Interferon

Interferon is a glycoprotein released by various cell types. Known molecules include IFN-α, IFN-β, and IFN-γ.

• IFN-α and IFN-β: Synthesized by many cell types in response to viral infection, their synthesis is induced by the presence of dsRNA. They inhibit viral replication, activate proteins that degrade viral nucleic acid, and increase the number of viral antigen-presenting proteins. This allows TCD8 lymphocytes (cytotoxic cells) and natural killer cells to rapidly degrade infected cells. Interferons bind to adjacent cell membranes, increasing resistance to infection in neighboring cells and isolating the infected area.
• IFN-γ: Released by tumor cells or cells infected by bacteria, its presence triggers the action of macrophages, killer cells, and TCD8 lymphocytes.