1. The ability of an animal to resist infection, to counter the harmful effects of toxins produced by infecting organisms, or to destroy cancer cells. Immunity in vertebrates depends on the presence in the body of a range of defensive cells and substances, notably antibodies and white blood cells (lymphocytes), which produce an immune response. Innate ( inherited or natural) immunity is the body’s first line of defence and plays a vital role in controlling invading organisms during the early stages of an infection. The entry of most potential pathogens is blocked by the body’s natural barrier defences, primarily the skin and the mucous membranes that line the digestive, respiratory, urinary, and reproductive tracts. Epithelial surfaces secrete mucus, which traps foreign particles, including microorganisms, while tears and saliva help to guard against entry via the eyes and mouth, aided by the enzyme lysozyme. In the airways a ciliated epithelium effectively sweeps away the mucus and trapped particles. Moreover, any pathogens entering in food must survive the highly acidic environment of the stomach. Pathogens that evade these physical and chemical barriers then face innate cellular defences. Macrophages, neutrophils, eosinophils, and certain other immune cells have cell surface receptors, called Toll-like receptors, that bind to common surface constituents of bacteria, viruses, fungi, and parasites. Such an encounter can prompt the macrophage to engulf the microorganism and to induce it to secrete an array of cytokines and chemokines. These substances attract additional immune cells to the site, including neutrophils and monocytes from nearby blood vessels, and initiate the process of inflammation. The complement system of defensive proteins is also activated; these coat target cells with fragments that assist recognition by macrophages. The abnormal surface proteins of virus-infected or cancerous cells may attract the attention of circulating natural killer cells, which release toxic chemicals that trigger programmed cell death. This innate response plays a crucial role in promoting adaptive (or acquired) immunity. Dendritic cells ingest foreign material, such as bacteria and virus particles (see antigen), and carry it to lymph organs, where they signal lymphocytes to carry out a more targeted and versatile repertoire of immune responses; adaptive immunity can persist throughout the lifetime of the individual. Active immunity arises when the body produces antibodies against an invading foreign substance (antigen), either through infection or immunization. Humoral immunity is when B lymphocytes produce free antibodies that circulate in the bloodstream (see b cell; b-cell receptor); cell-mediated immunity is caused by the action of T lymphocytes (see t cell; t-cell receptor). Passive immunity is induced by injection of serum taken from an individual already immune to a particular antigen; it can also be acquired by the transfer of maternal antibodies to offspring via the placenta or breast milk (see colostrum). Active immunity tends to be long-lasting (see immunological memory); passive immunity is short-lived. Invertebrates rely on innate defence mechanisms to combat invading pathogens, particularly the barrier of an external cuticle or exoskeleton, and multifunctional immune cells such as haemocytes. See also autoimmunity.

2. The condition induced in plants in response to infection by pathogens. Two broad lines of immune defence are recognized, both triggered by elicitor molecules derived either from the invading pathogen itself or from the breakdown of plant tissues arising from the infection. PAMP-triggered immunity (PTI) is a general immunity that arises from the interaction of transmembrane receptors (called pattern recognition receptors) in plant cells with elicitor molecules that characterize an entire category of pathogens. These are called pathogen-associated molecular patterns (PAMPs), a classic example being the chitin constituent of fungal cells walls. Effector-triggered immunity (ETI) is induced by elicitor molecules called effectors, specific to certain species or even strains of pathogens. These bind to R proteins in the cytoplasm of the plant cell and thereby trigger an immune response, which tends to be stronger than the PTI response; however, many of the effector pathways by which the plant responds are common to both, and the distinction is often blurred. In either case, receptor binding causes signal molecules to enter the cell nucleus and activate genes, resulting in production of defensive molecules that initiate various immune responses. These include the production of reactive oxygen species and nitric oxide, which are toxic to certain pathogens and also contribute to programmed cell death in the hypersensitive response, by which infected cells are sacrificed to save remaining healthy tissue. The deposition of polymers such as callose and lignin on the inside of cell walls acts to seal healthy cells from adjacent infected ones. Phytoalexins are nonspecific antimicrobial substances that can kill fungi and bacteria, and are also induced by viral infections and injury. Moreover, in both PTI and ETI a form of long-term immunity, called systemic acquired resistance, is initiated throughout the plant by the plant hormone salicylic acid.