Various danger signals can trigger the inflammatory reaction. These signals can come from foreign organisms but also from cells already present in the body: Following an attack, such as an injury for example, pathogens (bacteria, fungi, viruses, parasitic worms, etc.) can enter the body. These microorganisms have molecular patterns that are detected by the immune system: these are called danger signals. These molecular patterns are common to many microorganisms (components of the cell wall of bacteria and fungi, patterns in the genome of viruses, etc.). When a cell in the body accumulates mutations, it can transform into a cancer cell. Cancer cells have molecules on their surface that are recognized as danger signals by the immune system. Danger signals (present in particular on microorganisms or cancer cells) are recognized by certain immune cells, such as dendritic cells and mast cells. These cells constantly patrol the tissues; these are called sentinel cells. Sentinel cells detect danger signals using receptors on their plasma membrane. Following this recognition, the sentinel cells release molecules called: chemical mediators of inflammation (such as TNF, prostaglandins or histamine). The release of chemical mediators of inflammation causes: Dilation of blood vessels and blood flow to the affected site (explaining the swelling, redness and heat). The mass arrival of immune cells (granulocytes and monocytes) at the inflammatory site. These cells in turn release mediators allowing the recruitment of other immune cells. This is the phenomenon of amplification. The inflammatory reaction involves many molecules that cause the stereotypical symptoms of inflammation. The inflammatory reaction allows rapid response to danger signals, it is beneficial for the body. However, to stop excessive pain or when the inflammatory reaction causes tissue damage, anti-inflammatory drugs (such as aspirin, for example) are used. Anti-inflammatory drugs block the release or action of certain chemical mediators of inflammation. Thus, these drugs stop certain symptoms without preventing the inflammatory reaction from taking place. From birth, a child is able to defend itself against most attacks. This type of defense, genetically inherited, requiring no prior learning, is called an innate immune response. Innate immunity is based on non-specific recognition mechanisms. The molecules recognized are common to many pathogens (these are the danger signals, see 2.1). The modes of action of the innate immune response are stereotyped; they are identical regardless of the pathogen concerned. The inflammatory reaction is the first mechanism to be put in place; it is an innate response. The acute inflammatory reaction is the essential mechanism of innate immunity. Innate immunity is implemented very quickly. Innate immunity is the first to intervene in various situations (tissue damage, infection, cancer). Innate immunity is a first line of defense that initially acts alone and then continues throughout the immune response.