Unit Six. Animal Life
27. How the Animal Body Defends Itself
27.7. Active Immunity Through Clonal Selection
As we discussed earlier, B cells and T cells have receptors on their cell surfaces that recognize and bind to specific antigens. When a particular antigen enters the body, it must, by chance, encounter the specific lymphocyte with the appropriate receptor to provoke an immune response. The first time a pathogen invades the body, there are only a few B cells or T cells that may have the receptors that can recognize the invader’s antigens. Binding of the antigen to its receptor on the lymphocyte surface, however, stimulates cell division and produces a clone (a population of genetically identical cells). This process is known as clonal selection. For example, in the first encounter with a chicken pox virus in figure 27.13 there are only a few cells that can mount an immune response, and the response is relatively weak. This is called a primary immune response and is indicated by the first curve, which shows the initial amount of antibody produced upon exposure to the virus.
Figure 27.13. The development of active immunity.
Immunity to chicken pox occurs because the first exposure stimulated the development of lymphocyte clones with receptors for the chicken pox virus. As a result of clonal selection, a second exposure stimulates the immune system to produce large amounts of the antibody more rapidly than before, keeping the person from getting sick again.
If the primary immune response involves B cells, some of the cells become plasma cells that secrete antibodies (taking 10 to 14 days to clear the chicken pox virus from the system), and some become memory cells. Some of the T cells involved in the primary response also become memory cells. Because a clone of memory cells specific for that antigen develops after the primary response, the immune response to a second infection by the same pathogen is swifter and stronger, as shown by the second curve. Many memory cells can be produced following the primary response, providing a jump start for the production of antibodies should a second exposure occur. The next time the body is invaded by the same pathogen, the immune system is ready. As a result of the first infection, there is now a large clone of lymphocytes that can recognize that pathogen. This more effective response, elicited by subsequent exposures to an antigen, is called a secondary immune response. The “Inquiry and Analysis” feature at the end of this chapter further explores the nature of the secondary immune response.
Memory cells can survive for several decades, which is why people rarely contract chicken pox a second time after they have had it once. Memory cells are also the reason that vaccinations are effective. The viruses causing childhood diseases have surface antigens that change little from year to year, so the same antibody is effective for decades. Other diseases, such as influenza, are caused by viruses whose genes that encode surface proteins mutate rapidly. This rapid genetic change causes new strains to appear every year or so that are not recognized by memory cells from previous infections.
Although the cellular and humoral immune responses were discussed separately, they occur simultaneously in the body. The Key Biological Process illustration on the facing page follows the steps of a viral infection and shows how the cellular and humoral lines of defense work together to produce the body’s specific immune response.
When a virus invades the body, viral proteins are displayed on the surfaces of infected cells 1. Viruses and infected cells are taken up by macrophages through phagocytosis 2, and viral proteins are displayed on the surface of the macrophage attached to MHC proteins. Stimulated in this way, macrophages release interleukin-1 3. Interleukin-1 is an alarm signal that stimulates helper T cells 4. Activated helper T cells release interleukin-2, which triggers both the cellular (T cell) and humoral (B cell) responses 5. In the figure, the cellular response follows the green arrows, and the humoral response follows the red arrows.
While some activated T cells become memory T cells 5a that remain in the body and are able to more quickly fight future infections by the same virus, interleukin-2 also activates cytotoxic T cells. The cytotoxic T cells bind to infected cells that carry the viral antigen and kill them 6.
Interleukin-2 also activates B cells 7 that multiply in the cell. Some B cells become memory cells 8 that remain in the body for future infections by the same virus. Other activated B cells become plasma cells 9 that produce antibodies directed against the viral surface proteins. The antibodies released into the body will bind to viral proteins that are displayed on the surface of infected body cells 10 or that are present on the surface of the viruses. Cells or viruses that are tagged with antibodies are destroyed by macrophages that are circulating in the body 11. As you can see, both arms of the immune response work together very effectively to rid the body of invaders.
Key Learning Outcome 27.7. A strong immune response is possible because infecting cells stimulate the few responding B cells and T cells to divide repeatedly, forming clones of responding cells.