When we make an immune response to a given infectious agent, by definition that microorganism must exist in our environment and we are likely to meet it again. It would make sense then for the immune mechanisms alerted by the first contact with antigen to leave behind some memory system that would enable the response to any subsequent exposure to that particular antigen to be faster and greater in magnitude.
Our experience of many common infections tells us that this must be so. We rarely suffer twice from such diseases as measles, mumps, chickenpox, whooping cough, and so forth. The first contact clearly imprints some information, imparts some memory, so that the body is effectively prepared to repel any later invasion by that organism and a state of immunity is established.
Secondary immune responses are better
By following the production of antibody and of effector T‐cells on the first and second contacts with antigen, we can see the basis for the development of immunity. For example, when we inject a bacterial product such as tetanus toxoid into a rabbit, for the reasons already discussed, several days elapse before antibody production by B‐cells can be detected in the blood; these antibodies reach a peak and then fall (Figure 2.12). If we now allow the animal to rest and then give a second injection of toxoid, the course of events is dramatically altered. Within 2–3 days the antibody level in the blood rises steeply to reach much higher values than were observed in the primary immune response. This secondary immune response then is characterized by a more rapid and more abundant production of antibody resulting from the “tuning up” or priming of the antibody‐forming system. T‐lymphocytes similarly exhibit enhanced secondary responses, producing cells with improved helper or cytotoxic effector functions.
The fact that it is the lymphocytes that are responsible for immunological memory can be demonstrated by adoptive transfer of these cells to another animal, an experimental sys tem frequently employed in immunology. The immunological potential of the transferred cells is seen in a recipient treated with X‐rays that destroy its own lymphocyte population; thus the recipient animal acts as a living “test tube” in which the activity of the transferred lymphocytes can be assessed in vivo. Lymphocytes taken from an animal given a primary injection of antigen (for example, either tetanus toxoid or influenza hemagglutinin) and transferred to an irradiated host, which is then boosted with the same antigen, give a rapid, intense production of antibody characteristic of a secondary response (Figure 2.13a,d). To exclude the possibility that the first antigen injection might exert a nonspecific stimulatory effect on the lymphocytes, “criss‐cross” control animals are boosted by injection with a different antigen to that given for the primary injection. In these control animals only primary responses are seen to either antigen (Figure 2.13 b,c). We have explained the design of the study in detail to call attention to the need for careful selection of controls in immunological experiments.
The higher response given by a primed lymphocyte population is due to the presence of T and B memory cells which not only form a quantitatively expanded population of antigen‐specific lymphocytes (Figure 2.11) but also are functionally enhanced in comparison to the original naive lymphocytes from which they were derived.