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Adaptive immunity came into play relatively late in evolutionary terms, and is present only in vertebrates. Although an individual is born with the capacity to mount immune responses to foreign substances, the number of B and T cells available for mounting such responses must be expanded before one is said to be immune to that substance. This is achieved by activation of lymphocytes bearing antigen‐specific receptors following their contact with the antigen. Antigenic stimulation of B cells and T cells together with antigen‐presenting cells (APCs) initiates a chain of events that leads to proliferation of activated cells together with a program of differentiation events that generate the B‐ or T‐effector cells responsible for the humoral or cell‐mediated responses, respectively. These events take time to unfold (days to weeks). Fortunately, the cellular and noncellular components of the innate system are rapidly mobilized (minutes to hours) to eliminate or neutralize the foreign substance.

One way to think about this host defense strategy is to consider this as a one‐two punch launched initially by innate cells and noncellular elements of the immune system that are always available to quickly remove or cordon off the invader, followed by a round of defense that calls into play cells of the adaptive immune system (B and T cells) that are programmed to react with the foreign substance by virtue of their antigen‐specific receptors. Moreover, the clonal expansion of these cells—a process first explained by the clonal selection theory discussed in the section below—gives rise to an arsenal of antigen‐specific cells available for rapid responses to the same antigen in the future, a phenomenon referred to as memory responses. By this process, the individual acquires the immunity to withstand and resist a subsequent attack by, or exposure to, the same offending agent.

The discovery of adaptive immunity predates many of the concepts of modern medicine. It has been recognized for centuries that people who did not die from such life‐threatening diseases as bubonic plague and smallpox were subsequently more resistant to the disease than were people who had never been exposed to it. The rediscovery of adaptive immunity is credited to the English physician Edward Jenner who, in the late eighteenth century, experimentally induced immunity to smallpox. If Jenner performed his experiment today, his medical license would be revoked, and he would be the defendant in a sensational malpractice lawsuit. He inoculated a young boy with pus from a lesion of a dairy maid who had cowpox, a relatively benign disease that is related to smallpox. He then deliberately exposed the boy to smallpox. This exposure failed to cause disease! Because of the protective effect of inoculation with cowpox (vaccinia, from the Latin word vacca, meaning “cow”), the process of inducing adaptive immunity has been termed vaccination.

The concept of vaccination or immunization was expanded by Louis Pasteur and Paul Ehrlich almost 100 years after Jenner’s experiment. By 1900, it had become apparent that immunity could be induced against not only microorganisms but also their products. We now know that immunity can be induced against innumerable natural and synthetic compounds, including metals, chemicals of relatively low molecular weight, carbohydrates, proteins, and nucleotides.

The compound to which the adaptive immune response is induced is called an antigen, a term initially coined due to the ability of these compounds to cause antibody responses to be generated. Of course, we now know that antigens can generate antibody‐mediated (B cell‐derived) and T cell‐mediated responses.

Below we introduce the subject of the origins of B and T cells and other cells of the immune system in a process known as hematopoiesis.