Immunity: Active, Passive, and Delayed (World of Microbiology and Immunology)
Active, passive, and delayed immunity are all variations on the operation of the immune system, whereby antibodies are produced in response to the presence of an antigen considered to be foreign.
Active immunity occurs due to the production of an antibody as a result of the presence of the target antigen either as part of an intact infecting organism, or because of the introduction of the specific antigen in the form of a vaccine. The immunity is provided by an individual's own immune system.
The type of immunity invoked by the active response tends to be permanent. Once the antibody has been produced, an individual will be protected against the presence of the target antigen for a lifetime. The immune system has a capacity for memory of the antigen. If presented with the antigen challenge again, the immune machinery responsible for the formation of the corresponding antibody is rapidly triggered into action.
An example of active immunity is the injection into healthy individuals of the disabled toxins of bacteria such as Corynebacterium diphtheriae, the agent causing diphtheria, and Clostridium tetani, the agent that causes tetanus. This rational was first proposed by Paul Ehrlich. In 1927, Gaston Ramon attempted his suggestion. He separately injected inactivated version of the bacterial toxins and was able to demonstrate an immune response to both toxins. This rationale has carried forward to the present day. A combination vaccine containing both inactivated toxins is a routine inoculation in childhood.
Another historical development associated with active immunity involved Louis Pasteur. In 1884, Pasteur used weakened cultures of Bacillus anthracis, the causative agent of anthrax, and inactivated sample from the spinal cords of rabbits infected with the rabies virus to produce immunity to anthrax and rabies. Pasteur's method spurred the development of other active immune protective vaccines. Just one example is the oral poliomyelitis vaccine developed by Albert Sabin in the 1950s.
Passive immunity also results in the presence of antibody. However, the particular individual does not produce the antibody. Rather, the antibody, which has been produced in someone else, is introduced to the recipient. An example is the transfer of antibodies from a mother to her unborn child in the womb. Such antibodies confer some immune protection to the child in the first six months following birth. Indeed, the transient nature of the protection is a hallmark of passive immunity. Protection fades over the course of weeks or a few months following the introduction of the particular antibody. For example, a newborn carries protective maternal antibodies to several diseases, including measles, mumps and rubella. But by the end of the individual's first year of life, vaccination with the MMR vaccine is necessary to maintain the protection.
Another example of passive immunization is the administration to humans of tetanus antitoxin that is produced in a horse in response to the inactivated tetanus toxin. This procedure is typically done if someone has been exposed to a situation where the possibility of contracting tetanus exists. Rather than rely on the individual's immune system to respond to the presence of the toxin, neutralizing antibodies are administered right away.
Active and passive immunity are versions of what is known as antibody-mediated immunity. That is, antibodies bind to the antigen and this binding further stimulates the immune system to respond to the antigen threat. Antibodymediated immunity is also called humoral immunity.
A third type of immunity, which is known as delayed immunity or delayed-type hypersensitivity, is represents a different sort of immunity. Delayed immunity is a so-called cell-mediated immunity. Here, immune components called T-cells bind to the surface of other cells that contain the antigen on their surface. This binding triggers a further response by the immune system to the foreign antigen. The response can involve components such as white blood cells.
An example of delayed immunity is the tuberculin test (or the Mantoux test), which tests for the presence of Mycobacterium tuberculosis, the bacterium that causes tuberculosis. A small amount of bacterial protein is injected into the skin. If the individual is infected with the bacteria, or has ever been infected, the injection site becomes inflamed within 24 hours. The response is delayed in time, relative to the immediate response of antibody-based immunity. Hence, the name of the immunity.
See also Antibody formation and kinetics; Immunization