{"id":1199,"date":"2017-08-30T14:40:41","date_gmt":"2017-08-30T18:40:41","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/chapter\/21-7-transplantation-and-cancer-immunology\/"},"modified":"2018-06-25T18:30:22","modified_gmt":"2018-06-25T22:30:22","slug":"21-7-transplantation-and-cancer-immunology","status":"publish","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/chapter\/21-7-transplantation-and-cancer-immunology\/","title":{"raw":"21.7 Transplantation and Cancer Immunology","rendered":"21.7 Transplantation and Cancer Immunology"},"content":{"raw":"<div class=\"bcc-box bcc-highlight\">\r\n<h3>Learning Objectives<\/h3>\r\nBy the end of this section, you will be able to:\r\n<ul>\r\n \t<li>Explain the significance of the Rh factor in maternal-fetal blood type incompatability.<\/li>\r\n<\/ul>\r\n<\/div>\r\n<p id=\"fs-id2122116\">The immune responses to transplanted organs and to cancer cells are both important medical issues. With the use of tissue typing and anti-rejection drugs, transplantation of organs and the control of the anti-transplant immune response have made huge strides in the past 50 years. Today, these procedures are commonplace. <strong>Tissue typing<\/strong> is the determination of MHC molecules in the tissue to be transplanted to better match the donor to the recipient. The immune response to cancer, on the other hand, has been more difficult to understand and control. Although it is clear that the immune system can recognize some cancers and control them, others seem to be resistant to immune mechanisms.<\/p>\r\n\r\n<section id=\"fs-id1950171\">\r\n<h1>The Rh Factor<\/h1>\r\n<p id=\"fs-id1417330\">Red blood cells can be typed based on their surface antigens. ABO blood type, in which individuals are type A, B, AB, or O according to their genetics, is one example. A separate antigen system seen on red blood cells is the Rh antigen. When someone is \u201cA positive\u201d for example, the positive refers to the presence of the Rh antigen, whereas someone who is \u201cA negative\u201d would lack this molecule.<\/p>\r\n<p id=\"fs-id2158747\">An interesting consequence of Rh factor expression is seen in <strong>erythroblastosis fetalis<\/strong>, a hemolytic disease of the newborn (<a class=\"autogenerated-content\" href=\"#fig-ch22_07_01\">Figure 1<\/a>). This disease occurs when mothers negative for Rh antigen have multiple Rh-positive children. During the birth of a first Rh-positive child, the mother makes a primary anti-Rh antibody response to the fetal blood cells that enter the maternal bloodstream. If the mother has a second Rh-positive child, IgG antibodies against Rh-positive blood mounted during this secondary response cross the placenta and attack the fetal blood, causing anemia. This is a consequence of the fact that the fetus is not genetically identical to the mother, and thus the mother is capable of mounting an immune response against it. This disease is treated with antibodies specific for Rh factor. These are given to the mother during the subsequent births, destroying any fetal blood that might enter her system and preventing the immune response.<\/p>\r\n\r\n<figure id=\"fig-ch22_07_01\"><figcaption>\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"500\"]<img src=\"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/wp-content\/uploads\/sites\/149\/2017\/08\/2230_Erythroblastosis_Fetalis-3.jpg\" alt=\"This figure shows the progression of thedisease called erythroblastosis fetalis. The top panel shows the umbilical artery and vein and the placenta. The center panel shows the response in the immune system of a first Rh+ infant. The bottom panel shows the response in the case of a second exposure for a Rh+ infant.\" width=\"500\" height=\"1009\" \/> Figure 1. Erythroblastosis Fetalis. Erythroblastosis fetalis (hemolytic disease of the newborn) is the result of an immune response in an Rh-negative mother who has multiple children with an Rh-positive father. During the first birth, fetal blood enters the mother\u2019s circulatory system, and anti-Rh antibodies are made. During the gestation of the second child, these antibodies cross the placenta and attack the blood of the fetus. The treatment for this disease is to give the mother anti-Rh antibodies (RhoGAM) during the first pregnancy to destroy Rh-positive fetal red blood cells from entering her system and causing the anti-Rh antibody response in the first place.[\/caption]\r\n\r\n<\/figcaption><\/figure>\r\n<\/section><section id=\"fs-id1371098\">\r\n<h1>Tissue Transplantation<\/h1>\r\n<p id=\"fs-id2237570\">Tissue transplantation is more complicated than blood transfusions because of two characteristics of MHC molecules. These molecules are the major cause of transplant rejection (hence the name \u201chistocompatibility\u201d). <strong>MHC polygeny<\/strong> refers to the multiple MHC proteins on cells, and <strong>MHC polymorphism<\/strong> refers to the multiple alleles for each individual MHC locus. Thus, there are many alleles in the human population that can be expressed (<a class=\"autogenerated-content\" href=\"#tbl-ch22_08\">Table 8<\/a> and <a class=\"autogenerated-content\" href=\"#tbl-ch22_09\">Table 9<\/a>). When a donor organ expresses MHC molecules that are different from the recipient, the latter will often mount a cytotoxic T cell response to the organ and reject it. Histologically, if a biopsy of a transplanted organ exhibits massive infiltration of T lymphocytes within the first weeks after transplant, it is a sign that the transplant is likely to fail. The response is a classical, and very specific, primary T cell immune response. As far as medicine is concerned, the immune response in this scenario does the patient no good at all and causes significant harm.<\/p>\r\n\r\n<table id=\"tbl-ch22_08\" summary=\"\">\r\n<thead>\r\n<tr>\r\n<th colspan=\"3\">Partial Table of Alleles of the Human MHC (Class I) (Table 8)<\/th>\r\n<\/tr>\r\n<tr>\r\n<th>Gene<\/th>\r\n<th># of alleles<\/th>\r\n<th># of possible MHC I protein components<\/th>\r\n<\/tr>\r\n<\/thead>\r\n<tbody>\r\n<tr>\r\n<td>A<\/td>\r\n<td>2132<\/td>\r\n<td>1527<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>B<\/td>\r\n<td>2798<\/td>\r\n<td>2110<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>C<\/td>\r\n<td>1672<\/td>\r\n<td>1200<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>E<\/td>\r\n<td>11<\/td>\r\n<td>3<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>F<\/td>\r\n<td>22<\/td>\r\n<td>4<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>G<\/td>\r\n<td>50<\/td>\r\n<td>16<\/td>\r\n<\/tr>\r\n<\/tbody>\r\n<\/table>\r\n<table id=\"tbl-ch22_09\" summary=\"\">\r\n<thead>\r\n<tr>\r\n<th colspan=\"3\">Partial Table of Alleles of the Human MHC (Class II) (Table 9)<\/th>\r\n<\/tr>\r\n<tr>\r\n<th>Gene<\/th>\r\n<th># of alleles<\/th>\r\n<th># of possible MHC II protein components<\/th>\r\n<\/tr>\r\n<\/thead>\r\n<tbody>\r\n<tr>\r\n<td>DRA<\/td>\r\n<td>7<\/td>\r\n<td>2<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>DRB<\/td>\r\n<td>1297<\/td>\r\n<td>958<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>DQA1<\/td>\r\n<td>49<\/td>\r\n<td>31<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>DQB1<\/td>\r\n<td>179<\/td>\r\n<td>128<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>DPA1<\/td>\r\n<td>36<\/td>\r\n<td>18<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>DPB1<\/td>\r\n<td>158<\/td>\r\n<td>136<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>DMA<\/td>\r\n<td>7<\/td>\r\n<td>4<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>DMB<\/td>\r\n<td>13<\/td>\r\n<td>7<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>DOA<\/td>\r\n<td>12<\/td>\r\n<td>3<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>DOB<\/td>\r\n<td>13<\/td>\r\n<td>5<\/td>\r\n<\/tr>\r\n<\/tbody>\r\n<\/table>\r\n<p id=\"fs-id1949990\">Immunosuppressive drugs such as cyclosporine A have made transplants more successful, but matching the MHC molecules is still key. In humans, there are six MHC molecules that show the most polymorphisms, three class I molecules (A, B, and C) and three class II molecules called DP, DQ, and DR. A successful transplant usually requires a match between at least 3\u20134 of these molecules, with more matches associated with greater success. Family members, since they share a similar genetic background, are much more likely to share MHC molecules than unrelated individuals do. In fact, due to the extensive polymorphisms in these MHC molecules, unrelated donors are found only through a worldwide database. The system is not foolproof however, as there are not enough individuals in the system to provide the organs necessary to treat all patients needing them.<\/p>\r\n<p id=\"fs-id2229766\">One disease of transplantation occurs with bone marrow transplants, which are used to treat various diseases, including SCID and leukemia. Because the bone marrow cells being transplanted contain lymphocytes capable of mounting an immune response, and because the recipient\u2019s immune response has been destroyed before receiving the transplant, the donor cells may attack the recipient tissues, causing <strong>graft-versus-host disease<\/strong>. Symptoms of this disease, which usually include a rash and damage to the liver and mucosa, are variable, and attempts have been made to moderate the disease by first removing mature T cells from the donor bone marrow before transplanting it.<\/p>\r\n\r\n<\/section><section id=\"fs-id1707607\">\r\n<h1>Immune Responses Against Cancer<\/h1>\r\n<p id=\"fs-id1837177\">It is clear that with some cancers, for example Kaposi\u2019s sarcoma, a healthy immune system does a good job at controlling them (<a class=\"autogenerated-content\" href=\"#fig-ch22_07_02\">Figure 2<\/a>). This disease, which is caused by the human herpesvirus, is almost never observed in individuals with strong immune systems, such as the young and immunocompetent. Other examples of cancers caused by viruses include liver cancer caused by the hepatitis B virus and cervical cancer caused by the human papilloma virus. As these last two viruses have vaccines available for them, getting vaccinated can help prevent these two types of cancer by stimulating the immune response.<\/p>\r\n\r\n<figure id=\"fig-ch22_07_02\"><figcaption>\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"380\"]<img src=\"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/wp-content\/uploads\/sites\/149\/2017\/08\/2231_Kaposis_Sacroma_Lesions-3.jpg\" alt=\"This photograph shows lesions on the surface of skin.\" width=\"380\" height=\"675\" \/> Figure 2. Karposi\u2019s Sarcoma Lesions. (credit: National Cancer Institute)[\/caption]\r\n\r\n<\/figcaption><\/figure>\r\n<p id=\"fs-id2464332\">On the other hand, as cancer cells are often able to divide and mutate rapidly, they may escape the immune response, just as certain pathogens such as HIV do. There are three stages in the immune response to many cancers: elimination, equilibrium, and escape. Elimination occurs when the immune response first develops toward tumor-specific antigens specific to the cancer and actively kills most cancer cells, followed by a period of controlled equilibrium during which the remaining cancer cells are held in check. Unfortunately, many cancers mutate, so they no longer express any specific antigens for the immune system to respond to, and a subpopulation of cancer cells escapes the immune response, continuing the disease process.<\/p>\r\n<p id=\"fs-id2265552\">This fact has led to extensive research in trying to develop ways to enhance the early immune response to completely eliminate the early cancer and thus prevent a later escape. One method that has shown some success is the use of cancer vaccines, which differ from viral and bacterial vaccines in that they are directed against the cells of one\u2019s own body. Treated cancer cells are injected into cancer patients to enhance their anti-cancer immune response and thereby prolong survival. The immune system has the capability to detect these cancer cells and proliferate faster than the cancer cells do, overwhelming the cancer in a similar way as they do for viruses. Cancer vaccines have been developed for malignant melanoma, a highly fatal skin cancer, and renal (kidney) cell carcinoma. These vaccines are still in the development stages, but some positive and encouraging results have been obtained clinically.<\/p>\r\n<p id=\"fs-id1698041\">It is tempting to focus on the complexity of the immune system and the problems it causes as a negative. The upside to immunity, however, is so much greater: The benefit of staying alive far outweighs the negatives caused when the system does sometimes go awry. Working on \u201cautopilot,\u201d the immune system helps to maintain your health and kill pathogens. The only time you really miss the immune response is when it is not being effective and illness results, or, as in the extreme case of HIV disease, the immune system is gone completely.<\/p>\r\n\r\n<\/section>","rendered":"<div class=\"bcc-box bcc-highlight\">\n<h3>Learning Objectives<\/h3>\n<p>By the end of this section, you will be able to:<\/p>\n<ul>\n<li>Explain the significance of the Rh factor in maternal-fetal blood type incompatability.<\/li>\n<\/ul>\n<\/div>\n<p id=\"fs-id2122116\">The immune responses to transplanted organs and to cancer cells are both important medical issues. With the use of tissue typing and anti-rejection drugs, transplantation of organs and the control of the anti-transplant immune response have made huge strides in the past 50 years. Today, these procedures are commonplace. <strong>Tissue typing<\/strong> is the determination of MHC molecules in the tissue to be transplanted to better match the donor to the recipient. The immune response to cancer, on the other hand, has been more difficult to understand and control. Although it is clear that the immune system can recognize some cancers and control them, others seem to be resistant to immune mechanisms.<\/p>\n<section id=\"fs-id1950171\">\n<h1>The Rh Factor<\/h1>\n<p id=\"fs-id1417330\">Red blood cells can be typed based on their surface antigens. ABO blood type, in which individuals are type A, B, AB, or O according to their genetics, is one example. A separate antigen system seen on red blood cells is the Rh antigen. When someone is \u201cA positive\u201d for example, the positive refers to the presence of the Rh antigen, whereas someone who is \u201cA negative\u201d would lack this molecule.<\/p>\n<p id=\"fs-id2158747\">An interesting consequence of Rh factor expression is seen in <strong>erythroblastosis fetalis<\/strong>, a hemolytic disease of the newborn (<a class=\"autogenerated-content\" href=\"#fig-ch22_07_01\">Figure 1<\/a>). This disease occurs when mothers negative for Rh antigen have multiple Rh-positive children. During the birth of a first Rh-positive child, the mother makes a primary anti-Rh antibody response to the fetal blood cells that enter the maternal bloodstream. If the mother has a second Rh-positive child, IgG antibodies against Rh-positive blood mounted during this secondary response cross the placenta and attack the fetal blood, causing anemia. This is a consequence of the fact that the fetus is not genetically identical to the mother, and thus the mother is capable of mounting an immune response against it. This disease is treated with antibodies specific for Rh factor. These are given to the mother during the subsequent births, destroying any fetal blood that might enter her system and preventing the immune response.<\/p>\n<figure id=\"fig-ch22_07_01\"><figcaption>\n<figure style=\"width: 500px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/wp-content\/uploads\/sites\/149\/2017\/08\/2230_Erythroblastosis_Fetalis-3.jpg\" alt=\"This figure shows the progression of thedisease called erythroblastosis fetalis. The top panel shows the umbilical artery and vein and the placenta. The center panel shows the response in the immune system of a first Rh+ infant. The bottom panel shows the response in the case of a second exposure for a Rh+ infant.\" width=\"500\" height=\"1009\" \/><figcaption class=\"wp-caption-text\">Figure 1. Erythroblastosis Fetalis. Erythroblastosis fetalis (hemolytic disease of the newborn) is the result of an immune response in an Rh-negative mother who has multiple children with an Rh-positive father. During the first birth, fetal blood enters the mother\u2019s circulatory system, and anti-Rh antibodies are made. During the gestation of the second child, these antibodies cross the placenta and attack the blood of the fetus. The treatment for this disease is to give the mother anti-Rh antibodies (RhoGAM) during the first pregnancy to destroy Rh-positive fetal red blood cells from entering her system and causing the anti-Rh antibody response in the first place.<\/figcaption><\/figure>\n<\/figcaption><\/figure>\n<\/section>\n<section id=\"fs-id1371098\">\n<h1>Tissue Transplantation<\/h1>\n<p id=\"fs-id2237570\">Tissue transplantation is more complicated than blood transfusions because of two characteristics of MHC molecules. These molecules are the major cause of transplant rejection (hence the name \u201chistocompatibility\u201d). <strong>MHC polygeny<\/strong> refers to the multiple MHC proteins on cells, and <strong>MHC polymorphism<\/strong> refers to the multiple alleles for each individual MHC locus. Thus, there are many alleles in the human population that can be expressed (<a class=\"autogenerated-content\" href=\"#tbl-ch22_08\">Table 8<\/a> and <a class=\"autogenerated-content\" href=\"#tbl-ch22_09\">Table 9<\/a>). When a donor organ expresses MHC molecules that are different from the recipient, the latter will often mount a cytotoxic T cell response to the organ and reject it. Histologically, if a biopsy of a transplanted organ exhibits massive infiltration of T lymphocytes within the first weeks after transplant, it is a sign that the transplant is likely to fail. The response is a classical, and very specific, primary T cell immune response. As far as medicine is concerned, the immune response in this scenario does the patient no good at all and causes significant harm.<\/p>\n<table id=\"tbl-ch22_08\" summary=\"\">\n<thead>\n<tr>\n<th colspan=\"3\">Partial Table of Alleles of the Human MHC (Class I) (Table 8)<\/th>\n<\/tr>\n<tr>\n<th>Gene<\/th>\n<th># of alleles<\/th>\n<th># of possible MHC I protein components<\/th>\n<\/tr>\n<\/thead>\n<tbody>\n<tr>\n<td>A<\/td>\n<td>2132<\/td>\n<td>1527<\/td>\n<\/tr>\n<tr>\n<td>B<\/td>\n<td>2798<\/td>\n<td>2110<\/td>\n<\/tr>\n<tr>\n<td>C<\/td>\n<td>1672<\/td>\n<td>1200<\/td>\n<\/tr>\n<tr>\n<td>E<\/td>\n<td>11<\/td>\n<td>3<\/td>\n<\/tr>\n<tr>\n<td>F<\/td>\n<td>22<\/td>\n<td>4<\/td>\n<\/tr>\n<tr>\n<td>G<\/td>\n<td>50<\/td>\n<td>16<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<table id=\"tbl-ch22_09\" summary=\"\">\n<thead>\n<tr>\n<th colspan=\"3\">Partial Table of Alleles of the Human MHC (Class II) (Table 9)<\/th>\n<\/tr>\n<tr>\n<th>Gene<\/th>\n<th># of alleles<\/th>\n<th># of possible MHC II protein components<\/th>\n<\/tr>\n<\/thead>\n<tbody>\n<tr>\n<td>DRA<\/td>\n<td>7<\/td>\n<td>2<\/td>\n<\/tr>\n<tr>\n<td>DRB<\/td>\n<td>1297<\/td>\n<td>958<\/td>\n<\/tr>\n<tr>\n<td>DQA1<\/td>\n<td>49<\/td>\n<td>31<\/td>\n<\/tr>\n<tr>\n<td>DQB1<\/td>\n<td>179<\/td>\n<td>128<\/td>\n<\/tr>\n<tr>\n<td>DPA1<\/td>\n<td>36<\/td>\n<td>18<\/td>\n<\/tr>\n<tr>\n<td>DPB1<\/td>\n<td>158<\/td>\n<td>136<\/td>\n<\/tr>\n<tr>\n<td>DMA<\/td>\n<td>7<\/td>\n<td>4<\/td>\n<\/tr>\n<tr>\n<td>DMB<\/td>\n<td>13<\/td>\n<td>7<\/td>\n<\/tr>\n<tr>\n<td>DOA<\/td>\n<td>12<\/td>\n<td>3<\/td>\n<\/tr>\n<tr>\n<td>DOB<\/td>\n<td>13<\/td>\n<td>5<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p id=\"fs-id1949990\">Immunosuppressive drugs such as cyclosporine A have made transplants more successful, but matching the MHC molecules is still key. In humans, there are six MHC molecules that show the most polymorphisms, three class I molecules (A, B, and C) and three class II molecules called DP, DQ, and DR. A successful transplant usually requires a match between at least 3\u20134 of these molecules, with more matches associated with greater success. Family members, since they share a similar genetic background, are much more likely to share MHC molecules than unrelated individuals do. In fact, due to the extensive polymorphisms in these MHC molecules, unrelated donors are found only through a worldwide database. The system is not foolproof however, as there are not enough individuals in the system to provide the organs necessary to treat all patients needing them.<\/p>\n<p id=\"fs-id2229766\">One disease of transplantation occurs with bone marrow transplants, which are used to treat various diseases, including SCID and leukemia. Because the bone marrow cells being transplanted contain lymphocytes capable of mounting an immune response, and because the recipient\u2019s immune response has been destroyed before receiving the transplant, the donor cells may attack the recipient tissues, causing <strong>graft-versus-host disease<\/strong>. Symptoms of this disease, which usually include a rash and damage to the liver and mucosa, are variable, and attempts have been made to moderate the disease by first removing mature T cells from the donor bone marrow before transplanting it.<\/p>\n<\/section>\n<section id=\"fs-id1707607\">\n<h1>Immune Responses Against Cancer<\/h1>\n<p id=\"fs-id1837177\">It is clear that with some cancers, for example Kaposi\u2019s sarcoma, a healthy immune system does a good job at controlling them (<a class=\"autogenerated-content\" href=\"#fig-ch22_07_02\">Figure 2<\/a>). This disease, which is caused by the human herpesvirus, is almost never observed in individuals with strong immune systems, such as the young and immunocompetent. Other examples of cancers caused by viruses include liver cancer caused by the hepatitis B virus and cervical cancer caused by the human papilloma virus. As these last two viruses have vaccines available for them, getting vaccinated can help prevent these two types of cancer by stimulating the immune response.<\/p>\n<figure id=\"fig-ch22_07_02\"><figcaption>\n<figure style=\"width: 380px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/wp-content\/uploads\/sites\/149\/2017\/08\/2231_Kaposis_Sacroma_Lesions-3.jpg\" alt=\"This photograph shows lesions on the surface of skin.\" width=\"380\" height=\"675\" \/><figcaption class=\"wp-caption-text\">Figure 2. Karposi\u2019s Sarcoma Lesions. (credit: National Cancer Institute)<\/figcaption><\/figure>\n<\/figcaption><\/figure>\n<p id=\"fs-id2464332\">On the other hand, as cancer cells are often able to divide and mutate rapidly, they may escape the immune response, just as certain pathogens such as HIV do. There are three stages in the immune response to many cancers: elimination, equilibrium, and escape. Elimination occurs when the immune response first develops toward tumor-specific antigens specific to the cancer and actively kills most cancer cells, followed by a period of controlled equilibrium during which the remaining cancer cells are held in check. Unfortunately, many cancers mutate, so they no longer express any specific antigens for the immune system to respond to, and a subpopulation of cancer cells escapes the immune response, continuing the disease process.<\/p>\n<p id=\"fs-id2265552\">This fact has led to extensive research in trying to develop ways to enhance the early immune response to completely eliminate the early cancer and thus prevent a later escape. One method that has shown some success is the use of cancer vaccines, which differ from viral and bacterial vaccines in that they are directed against the cells of one\u2019s own body. Treated cancer cells are injected into cancer patients to enhance their anti-cancer immune response and thereby prolong survival. The immune system has the capability to detect these cancer cells and proliferate faster than the cancer cells do, overwhelming the cancer in a similar way as they do for viruses. Cancer vaccines have been developed for malignant melanoma, a highly fatal skin cancer, and renal (kidney) cell carcinoma. These vaccines are still in the development stages, but some positive and encouraging results have been obtained clinically.<\/p>\n<p id=\"fs-id1698041\">It is tempting to focus on the complexity of the immune system and the problems it causes as a negative. The upside to immunity, however, is so much greater: The benefit of staying alive far outweighs the negatives caused when the system does sometimes go awry. Working on \u201cautopilot,\u201d the immune system helps to maintain your health and kill pathogens. The only time you really miss the immune response is when it is not being effective and illness results, or, as in the extreme case of HIV disease, the immune system is gone completely.<\/p>\n<\/section>\n","protected":false},"author":10,"menu_order":8,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":[],"pb_section_license":""},"chapter-type":[],"contributor":[],"license":[],"class_list":["post-1199","chapter","type-chapter","status-publish","hentry"],"part":1155,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/wp-json\/pressbooks\/v2\/chapters\/1199","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/wp-json\/wp\/v2\/users\/10"}],"version-history":[{"count":1,"href":"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/wp-json\/pressbooks\/v2\/chapters\/1199\/revisions"}],"predecessor-version":[{"id":1560,"href":"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/wp-json\/pressbooks\/v2\/chapters\/1199\/revisions\/1560"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/wp-json\/pressbooks\/v2\/parts\/1155"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/wp-json\/pressbooks\/v2\/chapters\/1199\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/wp-json\/wp\/v2\/media?parent=1199"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/wp-json\/pressbooks\/v2\/chapter-type?post=1199"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/wp-json\/wp\/v2\/contributor?post=1199"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/dcbiol11031109\/wp-json\/wp\/v2\/license?post=1199"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}