You have seen in this chapter that lasting immunity against a pathogen can be achieved in two ways, both of which involve exposure to an antigen associated with the pathogen and the resulting production of memory cells. The first way is natural: In Investigating Life: What Are the Mechanisms and Implications of Long Lasting Immunity?, we showed that people exposed to virulent strains of flu viruses retain their immunity, and even increase it when exposed to less harmful flu strains. The second way is artificial: As we described in the opening story, vaccines have been spectacularly successful at inducing lasting immunity and even eradicating diseases when enough people are vaccinated. Why, then, do people refuse vaccination? There appear to be several reasons. One is complacency—the threat of disease may seem remote. For example, measles, which used to kill thousands of children every year in the United States and still does in poor countries, is no longer a highly visible threat to public health. Second, some people believe that vaccines, although exhaustively tested and proven safe, are actually unsafe and cause disease. The internet is full of such assertions. Third, false alarms have led people to dismiss vaccination advisories. The discovery of the H1N1 flu virus (swine flu) in Mexico in 2009 led to a high alert and a mass vaccination program that turned out not to be necessary. In addition, some people are suspicious of governmental programs in general. In Pakistan, a polio vaccination program was used as a ruse by officials to gain access to the home of the international terrorist Osama bin Laden. Vaccination is a scientific success in terms of bolstering immunity and eradicating disease. But like any technology, its acceptance is a political issue.
Following activation of the immune system, many effector cells are mobilized. Most eventually die, but some survive as memory cells. Researchers are investigating how this happens. At the University of Wisconsin, Marulasiddappa Suresh and his colleagues have shown that a single transcription factor called FoxO1 plays an important role in the effector-to-memory-cell transition. This molecule is not needed for the production of effector cells, but if it is not there, memory cells do not form. The genes regulated by FoxO1 are being characterized and may hold the key to the memory cell. Meanwhile, at Yale University, Susan Kaech and her colleagues have shown that an intercellular signaling molecule, interleukin-7 (IL-7), binds to effector cells and results in changes that may allow memory cell survival. Specifically, the target cells produce a membrane channel that allows rapid uptake of glycerol, the backbone of fats. Production of fats in the memory cell may provide the energy needed for long-term survival. Understanding how memory cells form and survive may provide valuable information for the production of better vaccines.