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Chapter 20 : Immunity

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Immunity, Page 1 of 2

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Abstract:

A short history of tumor immunology is presented in this chapter. Although the evidence for tumor-specific transplantation antigens accumulated in experimental models, tumor-specific immunity in humans remained controversial. Some human tumors have tumor antigens detectable by in vitro assays. Several human tumor-specific antigens have been identified by these assays. Therefore, most of the data in which in vitro human tumor immunity was tested using cell lines is now being reinterpreted. If the immune system is playing a prominent role in the development of cancers, then agents that cause cancer (carcinogens) would be expected to be immunosuppressive, and immunosuppressive agents would be expected to be carcinogenic. Tumor tissue is often infiltrated by large numbers of lymphocytes, perhaps because of a cellular immunologic reaction to tumor antigens. Properties of cells mediating tumor immunity, and the major oncogenes and their products under study as determinants of prognosis in human cancer are listed. More recently, new tumor antigens identified both serologically (SEREX) and by reactivity of cell lines from patients to tumors, genetically modified cells expressing these antigens, as well as a variety of adjuvants, including liposomes, cytokines, conjugates, viral vectors, bacillus Calmette-Guérin (BCG), and dendritic cell processing, are now being tested in clinical trials. Understanding and control of these phenomena may result in effective immunotherapy of cancer in humans. The chapter ends with the history of immunotherapy of cancer.

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Figure 20.1

Some antigenic features of tumor cells. Some antigenic changes in tumors include loss or gain of major histocompatibility complex (MHC) antigens, loss or gain of carbohydrates (CHO), appearance of virus-associated tumor antigens (TAVA), tumor-associated transplantation antigens shared by different tumors (TATA), tumor-specific transplantation antigens essentially unique for a given tumor (TSTA), and markers shared by embryonic tissues and tumors (oncodevelopmental antigens [ODA]).

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Figure 20.2

Demonstration of specific rejection of an autochthonous tumor. A chemically induced primary tumor is induced in mouse A and then removed surgically. Asuspension of the tumor cells is made, and a transplantable dose of tumor cells is injected back into mouse A as well as into a normal syngeneic mouse of the same strain (B). The tumor grows in mouse B but not in the original primary tumor-bearing animal (autochthonous host). Thus, mouse A, the animal in which the tumor arose, has developed immune resistance to the growth of its own tumor. However, the tumor will grow when injected into a normal, previously unexposed recipient of the same strain (mouse B). On the other hand, a second tumor arising in another individual of the same strain (mouse C) will grow when injected into the animal in which the first tumor was produced (mouse A). Thus, the tumor resistance shown in mouse A is specific for the first tumor induced in mouse A and does not extend to other tumors (TSTA). This experiment demonstrates that an individual can develop specific immunity to an autochthonous tumor.

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Figure 20.3

Winn assay. To determine the effect of a given cell population on the viability of tumor cells, the effector cells (lymphoid cells) are admixed in vitro with the tumor target cells, and the mixture of cells is transplanted into a normal syngeneic recipient. If growth of the tumor is inhibited in comparison to tumor cells alone or tumor cells treated with control (unsensitized) lymphoid cells, it may be concluded that the effector lymphoid cell population has adversely affected the tumor cells.

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Figure 20.4

Activation of CD8+ cytotoxic T cells requires two signals: T-cell receptor reacting with antigen presented by MHC class I molecule and interaction of CD28 with B7 on the tumor cell. Tumor cells that lack B7 will not activate CD8+ precytotoxic cells. The same tumor cell transfected with B7 will activate TCTL cells, which will kill target cells that do not express B7. Interaction of T-cell receptor with antigen on MHC class I in the absence of costimulatory signals results in inactivation of the CD8+ precytotoxic cells.

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Figure 20.5

Oncodevelopmental markers. Various oncodevelopmental markers are normally expressed at different stages of neonatal development and by proliferating tissues in the adult. The T—locus markers of the mouse and other differentiation antigens may be expressed on germinal cells and in the preimplantation embryo, as well as in primitive tumors of embryonal stem cells, teratocarcinomas. Oncogene products are expressed during development and in tumors. Placental hormones, isoenzymes, and proteins may be expressed in adult tumors of testes, ovary, liver, and breast. Other markers, such as alpha—fetoprotein (AFP) and carcinoembryonic antigen (CEA), are produced normally by developing liver or colonic mucosal cells, respectively, and are frequently expressed in tumors of these tissues, i.e., hepatocellular carcinomas and adenocarcinomas of the colon, as well as in other tumors of embryologically related tissues. Immunoglobulins and lymphocyte differentiation markers (CDs) are found to be associated with lymphoproliferative tumors. Many surface glycoprotein and glycolipid carbohydrate differences recognized by monoclonal antibodies are due to the activity of glycosylating enzymes in tumors that are normally active during normal development. Gene rearrangements that occur normally during plasma cell development are used to identify clonality and B—cell origin of lymphoid tumors.

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Figure 20.6

Representative changes in the concentration of AFP in serum in response to therapy. Successful treatment is reflected in a rapid fall of the serum concentration to normal. If the concentration does not fall rapidly or becomes reelevated, tumor is still present.

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Figure 20.7

Cell surface carbohydrate structures. Cell surface carbohydrates are synthesized from a common Gal—Glu disaccharide by addition of linear or branched monosaccharides. The four major classes are ganglio, globo, lacto—type 1, and lacto—type 2. (From S. Sell, Hum. Pathol. 21:1003—1990.)

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Figure 20.8

Carbohydrate structure of some major human cancer markers recognized by MAbs. The epitope designated SLEX (sialylated Lewis X, also known as SSEA or LEX) is formed by fucosylation of the type 2 lacto chain. CA 50 is formed by sialylation of the type 1 lacto chain, and CA 19—9 (Sialyl Leal) is formed by fucosylation of CA 50. The Forssman antigen is not found normally on human cells but may be identified on cancer cells because of an increase in expression of Nacetylgalactosamine transferase, producing the Forssman pentasaccharide in the globo series. OFA—2 (oncofetal antigen 2) is produced by addition of the N—acetygalactosamine to the core trisaccharide of the globo series; OFA—1 is produced by sialylation of OFA—2. (From S. Sell, Hum. Pathol. 21:1003—1019, 1990.)

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Figure 20.9

Cancer-associated ganglio chains. Monoclonal antibodies to epitopes of the ganglio series have a high specificity for the terminal sialic acid (NeuNAC) residues produced by increased sialylation of the ganglio chains. The additional monosaccharide added to produce a new epitope is indicated by slanted lines.

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Tables

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Table 20.1

A short history of tumor immunity

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.2

Evidence for tumor immunity in humans

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.3

Terminology of host-tumor graft relationships

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.4

Immunogenicity of rat tumors a

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.5

Some in vitro assays for tumor antigens

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
Generic image for table
Table 20.6

Properties of cells mediating tumor immunity

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
Generic image for table
Table 20.7

Factors responsible for failure of immune surveillance of cancer

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
Generic image for table
Table 20.8

Some clinical applications of cancer markers a

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.9

Some types of cancer markers

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.10

Levels of expression of oncodevelopmental markers by tumors

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.11

CEA concentrations in human sera a

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.12

Cancer markers in clinical use a

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.13

CD antigens on lymphoid tumors

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.14

Comparison of CEA, CA 19-9, CA 50, and CA 242 in patients with colorectal or pancreatic-biliary cancer

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.15

Percentages of patients with elevated serum HCG or AFP in germ cell tumors

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.16

Cytoskeletal elements in cancers

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.17

Oncogene products being considered as candidates for tumor markers

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.18

Immunotherapeutic approaches to human cancer

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.19

Clinical trials: definitions

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.20

Problems and possible solutions to MAb immunotherapy of cancer in humans

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.21

Strategy for development of MAbs for cancer immunotherapy

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.22

Some examples of preclinical trials in mice of immune gene therapy for cancer a

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.23

Some antigens on human tumors recognized by antibody or T-cell reactions

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20
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Table 20.24

Some techniques to induce tumor immunity (tumor vaccines)

Citation: Sell S. 2001. Immunity, p 628-682. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch20

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