2.5 The Cellular Immune Response
As the fruit picking was going on, Brian heard someone shout, “Bless you!” after a fellow fruit-picker let out a loud sneeze. Unbeknownst to poor little Brian, some of the air he was breathing in the orchard was now laden with particles of the influenza virus. While the humoral immune response is underway, some of the influenza viral particles will have been consumed by phagocytes and neutrophils while others would have began infecting other cells such as Brian’s epithelial cells. So, how does the immune system deal with these infected cells? By a battle plan called the cellular immune response. Like the humoral immune response, this is also divided into activation and effector phases. The activation phase begins when an antigen-presenting cell (APC) of the host organism encounters and attacks an invading virus. Meanwhile, other viruses look for nearby epithelial cells to infect. A lysosome containing digestive enzymes combines with the phagosome to process the antigens. The processed antigens combine with MHC class II proteins and are presented on the surface of the APC. The virus also infects Brian’s epithelial cells. Within the infected epithelial cells the virus is processed, attached to an MHC class I protein and is presented on the cell surface. A helper T cell (CD4+) recognizes the displayed antigen on the APC and binds to the MHC class II protein-antigen complex. The activated helper T cell releases chemical messengers such as the cytokine IL-2 and gamma interferon (IFN-g).

The effector phase begins when activated cytotoxic T cells (CD8+) which were stimulated to proliferate by the cytokine IL-2, recognize the MHC class I protein-antigen complex on the infected epithelial cells. Cytokines also attract other killer T cells to the site of infection. The activated cytotoxic T cell binds to the MHC class I protein-antigen complex on the surface of the infected epithelial cell. The binding causes the cytotoxic T cell to release a potent chemical called perforin. Perforin perforates the cell membrane of the infected cells causing the cells to lyse (burst) and die. As the viral infection is brought under control, regulatory T cells turn off the activated cytotoxic T cells. Memory T cells remain behind to respond quickly if the same virus attacks again.

Figure 4. The cellular immune response.

Finally, as the infection in Brian’s thumb is brought under control, yet another type of T cell, the regulatory T cell, instructs the activated combat units consisting of B cells, helper T cells, and killer T cells to switch from battle mode to stand-by mode. Most of these immune cells will die, but a few will live to fight another day. These cells, called memory cells, will be able to respond more quickly the next time Brian is unfortunate enough to be invaded by the same strain of bacteria. The above account highlights the overwhelming reliance that our body places on the T cell to fight off microbial infections. But accidents do happen (as it is in life in general) within the immune system and sometimes these cells mistake part of our body (self) for a microbe (non-self) and the resulting “friendly fire” can lead to autoimmune diseases such as multiple sclerosis and juvenile diabetes. To avoid this kind of “collateral damage” nascent T cells are subjected to a strict training program in the thymus. As part of their education, the developing T cells are exposed to as many self-proteins as possible and any T cell that displays any reactivity is eliminated. This rigorous training regime ensures that the remaining T cells will react only to non-self molecules.

Although the foregoing description of the immune response applies mainly to viruses and bacteria, it is important to note that the immune system reacts in a similar manner when it encounters cancer cells, which it also recognizes as foreign or “non-self” and therefore, must destroy. Scientists have observed in the laboratory that the cells and other components of the immune system are capable of destroying malignant tumor cells. They have found that certain antibodies that recognize tumor cells help the macrophages and the natural killer cells to accomplish their mission. Over the years, further study of the immune system has demonstrated that the body defends itself against cancer in much the same way that it seeks to eliminate other intruders such as bacteria and viruses. Further study of the immune system is expected to reveal ways to bolster it, allowing the body to become a more active partner in the fight against cancer.

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