McKenna's Pharmacology for Nursing, 2e

C H A P T E R 1 5  Introduction to the immune response and inflammation 235

• IgE is present in small amounts and seems to be related to allergic responses and to the activation of mast cells. • IgD is another identified immunoglobulin whose role has not been determined. This process of antibody formation, called acquired or active immunity, is a lifelong reaction. For example, a person exposed to chickenpox will have a mild res­ piratory reaction when the virus (varicella) first enters the respiratory tract. There will then be a 2- to 3-week incubation period as the body is forming IgM anti­ bodies and preparing to attack any chickenpox virus that appears. The chickenpox virus enters a cell and multiplies. The cell eventually ruptures and ejects more viruses into the system. When this happens, the body responds with the immediate release of antibodies, and a full scale antigen–antibody response is seen throughout the body. Fever, myalgia, arthralgia and skin lesions are all part of the immune response to the virus. Once all of the invading chickenpox viruses have been destroyed or have entered the CNS to safely hibernate away from the antibodies, the clinical signs and symptoms resolve. (Varicella can enter the CNS and stay dormant for many years. The antibodies are not able to cross into the CNS, and the virus remains unaffected while it stays there.) The B memory cells will continue to make a supply of immunoglobulin, IgG, for use on future exposure to the chickenpox virus. That exposure does not usually evolve into a clinical case because the viruses are destroyed immediately on entering the body and do not have a chance to multiply. Older people with weakened immune systems, people who are immunosuppressed and indi­ viduals who have depleted their immune system fighting an infection are at risk for development of shingles if they had chickenpox earlier in their lives. The dormant virus, which has aged and changed somewhat, is able to leave the CNS along a nerve root because the immuno­ suppressed body is slow to respond. The antibodies do eventually respond to the varicella, and the signs and symptoms of shingles occur as the virus is attacked along the nerve root. Figure 15.5 outlines this entire process. B clones cluster in areas where they are most likely to encounter the specific antigen that they have been programmed to recognise. For example, pathogens or antigens that are introduced into the body via the res­ piratory tract will meet up with the B cells in the tonsils and upper respiratory tract; antigens that enter the body through the GI tract will meet their B cells situated in the oesophagus and GI tract. Theorists believe that the B cells are programmed genetically and are formed by the time of birth. Clones of B cells contain similar cells. The introduction of an antigen to which there are no pre­ programmed B cells could result in widespread disease because the body would have no way of responding. A major concern about space travel has always been the

introduction of a completely new antigen to Earth; for this reason, long periods of decontamination have been used after rocks or debris are brought back to Earth. Germ warfare research is ongoing in some countries to develop an antigen that has not been seen before and to which people would have no response. Other mediators Several other factors also play an important role in the immune reaction. Interferons are chemicals that are secreted by cells that have been invaded by viruses and possibly by other stimuli. The interferons prevent viral replication and also suppress malignant cell replication and tumour growth. Interleukins are chemicals secreted by active leuco­ cytes to influence other leucocytes. Interleukin 1 (IL-1) stimulates T and B cells to initiate an immune response. IL-2 is released from active T cells to stimulate the pro­ duction of more T cells and to increase the activity of B cells, cytotoxic cells and natural killer cells. Interleu­ kins also cause fever, arthralgia, myalgia and slow-wave sleep induction—all things that help the body to conserve energy for use in fighting off the invader. Several other factors released by lymphocytes and basophils have been identified. These include interleukins such as B-cell growth factor, macrophage-activating factor, macrophage inhibiting factor, platelet-activating factor, eosinophil chemotactic factor and neutrophil chemotactic factor. The thymus gland also releases a number of hormones that aid in the maturation of T cells and that circulate in the body to stimulate and communicate with T cells. Thymosin, a thymus hormone that has been rep­ licated, is important in the maturation of T cells and cell-mediated immunity. Research is ongoing on the use of thymosin in certain leukaemias and melanomas to stimulate the immune response. Tumour necrosis factor (TNF), a cytokine, is a chemical released by macrophages that inhibits tumour growth and can actually cause tumour regression. It also works with other chemicals to make the inflam­ matory and immune responses more aggressive and efficient. Research is ongoing to determine the thera­ peutic effectiveness of TNF. TNF receptor sites are now available for injection into people with acute rheumatoid arthritis. These receptor sites react with TNF released by the macrophages in this inflammatory disease. All of these chemicals act as communication factors within the immune system, allowing the coordination of the immune response. Interrelationship of the immune and inflammatory responses The immune and inflammatory responses work together to protect the body and to maintain a level of homeo­ stasis. Helper T cells stimulate the activity of B cells and