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Chapter 17 : Immunoproliferative Diseases

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Abstract:

Immunoproliferative diseases include both inflammatory (self-limited, reversible) and malignant (progressive) increases in numbers of cells. The identification of cell surface markers for various lymphocyte populations has led to a much better understanding of lymphocyte differentiation and to the reclassification of immunoproliferative diseases on the basis of T-cell, B-cell, or macrophage (histiocyte) lineage. Lymphomas and leukemias are progressively growing tumors that mimic the appearance normal lymphoid cells. These tumors are now classified as poorly differentiated forms of diffuse B-cell lymphoma. A diagram of the normal maturation of blood cells with the stages of development at which maturation arrest becomes manifest for various leukemias and lymphomas is presented in this chapter. Human lymphomas are cancers of lymphoid cells: T cells, B cells, or macrophages. The major clinical classification consists of two types, non-Hodgkin's and Hodgkin's lymphoma, because the response to therapy and clinical course of Hodgkin’s diseases and other lymphomas are critically different. Three major characteristics determine the ability to predict the growth behavior of a malignant lymphoma, non-Hodgkin’s type: the pattern of tissue replacement, the morphology of the cells, and the extent of organ involvement. The chapter uses a simplified classification of B-cell, T-cell, and macrophage tumors which is relatively easy to understand. The major characteristics of some B-cell tumors are listed in this chapter. Patients with lymphoproliferative disease are subject to an increased incidence of clinically significant infections.

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
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Image of Figure 17.1
Figure 17.1

Maturation of blood cells during hematopoiesis and postulated sites of maturation arrest in lymphomas and leukemias. (1) Acute undifferentiated leukemia. (2) Acute lymphocyte leukemia. (3) T-cell leukemia (acute lymphocytic leukemia) (in blood), T-cell lymphoma (in tissues). (4) B-cell leukemia (acute lymphocytic leukemia, chronic lymphocytic leukemia) (in blood), B-cell lymphoma (in tissues), multiple myeloma (in plasma cells), Hodgkin's disease (lymphocyte predominant). (5) Polycythemia rubra vera. (6) Acute erythroid leukemia. (7) Acute myeloblastic leukemia. (8) Chronic granulocytic leukemia. (9) Monocytic leukemia (in blood), true histiocytic lymphoma (in tissue), Hodgkin's disease (other types). (10) Acute megakaryocyte leukemia.

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
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Image of Figure 17.2
Figure 17.2

Structure of lymph node and origin of lymphomas. Drawing of lymph node illustrating anatomic localization of B cells (follicles), T cells (diffuse, paracortex, and deep cortex) and macrophages (medullary cords). B-cell tumors arise in the cortex and are often follicular in structure but sometimes diffuse. T-cell lymphomas arise in the paracortex and deep cortex and are always diffuse. Tumors of macrophages arise in the medulla and are diffuse. In general, the structure of the tumor reflects the normal morphology of the cell type from which it arises. (Modified from R. S. Mann, E. S. Jaffe, and C. W. Berard, Am. J. Pathol. 94:105–192, 1979.)

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
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Image of Figure 17.3
Figure 17.3

Histologic features of B-cell lymphomas as related to morphology of germinal center B cells. During the cell cycle, B cells change from small round cells to large “blast cells” and divide to form small cells. Differentiation results in production of plasma cells. The nucleus of the early activated B cell is cleaved, whereas the nuclei of the small resting cell and the cells in later stages of B-cell differentiation are not cleaved. Chronic lymphocyte leukemia represents a maturation arrest at the small noncleaved stage; multiple myeloma at the plasma cell stage; follicular lymphomas at the activated B-cell stage (cleaved), and large-cell lymphomas at the immunoblastic B-cell stage (large noncleaved cells). (Modified from R. J. Lukes and R. D. Collins, Cancer Treatment Rep. 61:971–979, 1977, and C. R. Taylor, Arch. Pathol. Lab. Med. 102:549–554, 1978.)

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
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Image of Figure 17.4
Figure 17.4

Patterns of normal polyclonal and neoplastic B-cell follicles. Normal secondary or germinal centers contain a mixture of different cell types, including not only polyclonal B cells but also macrophages and T cells, and are surrounded by a rim of polyclonal cells. On the other hand, malignant B-cell tumors may form follicles or replace the node structure diffusely with a homogeneous cell type. Malignant follicles are made up of cells of a single clonal line, do not contain T cells or macrophages, and are not surrounded by a rim of polyclonal cells. Malignant follicles efface the other components of the lymph node (paracortex, medulla) and extend diffusely into adjacent tissue, with loss of the structure of capsule and subcapsular sinus, whereas in nonmalignant hyperplasia, these areas, although relatively less conspicuous, are preserved.

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
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Image of Figure 17.5
Figure 17.5

Evolution of B-cell lymphomas. Increased malignancy or the progression toward more aggressive tumor is associated with a change from more follicular to more diffuse, as well as with cell size and morphology. Small, cleaved follicular tumors have the best prognosis. Large, noncleaved diffuse tumors have the worst prognosis. Approximately 30% of patients followed carefully demonstrate progression from less malignant to more malignant forms.

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
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Image of Figure 17.6
Figure 17.6

Expression of CD markers during B-cell development and on B-cell tumors. (i) Stem cell: CDs 19 and 38; sometimes CDs 22 and 24; no Ig gene rearrangements; no Ig expression. (ii) Pre-pre-B cell: gain of CD 10; VDJCμ rearrangement; no Ig expression. (iii) Pre-B cell: same CDs as above; VDJCμ rearrangement; cytoplasmic μ chain. (iv) Early B cell: loss of CD 10 and 38, gain of CD 21 and 39; μ or μ and δ surface positive. (v) Late B cell: loss of CD 21, gain of CDs 23 and 38; VDJC class gene rearrangements; μ, γ, ϵ, or δ surface positive. (vi) Plasma cell: loss of CDs 19, 22, 23, and 24; gain of PCA1 (plasma cell antigen 1); cytoplasmic Ig of a single class. The expression of these markers on various B-cell tumors is indicated at the bottom of the figure.

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
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Image of Figure 17.7
Figure 17.7

T-cell differentiation markers and T-cell lymphomas. The boxes in the top half of the figure indicate the appearance of T-CLL markers detected by monoclonal antibodies at the stages of normal T-cell development. The boxes in the bottom half of the figure indicate the expression of these markers on T-cell tumors.

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
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Image of Figure 17.8
Figure 17.8

Reed-Sternberg cells are large multinucleated “giant” cells considered essential for the diagnosis of Hodgkin's disease.

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
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Image of Figure 17.9
Figure 17.9

Drawing of cell types in Hodgkin's disease. Depicted is a drawing modified from a textbook by William Osler published in 1914, illustrating the different cell types seen in mixed-cellularity Hodgkin's disease. The diagnosis depends on the identification of Reed-Sternberg cells in a lesion containing a mixture of other cell types. Lymphocytes and eosinophils are often prominent.

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
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Image of Figure 17.10
Figure 17.10

Clinical staging of Hodgkin's disease. Staging correlates well with prognosis and helps in deciding the selection of therapy. The same clinical staging is also applicable to the non-Hodgkin's lymphomas. Stage I: involvement of a single lymph node region. Stage II: involvement of two or more lymph node regions on the same side of the diaphragm. Stage III: involvement of lymphatic structures on both sides of the diaphragm. Stage IV: diffuse or disseminated involvement.

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
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Image of Figure 17.11
Figure 17.11

Diagram of the t(8;14) translocation in Burkitt's lymphoma cells. The c-myc gene on chromosome 8 translocates next to the C and Cγ genes on chromosome 14. (From J. Erikson, A. ar-Rushdi, H. L. Drwinga, P. C. Nowell, and C. M. Croce, Proc. Natl. Acad. Sci. USA 80:820–824, 1983.)

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
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Tables

Generic image for table
Table 17.1

Nonmalignant lymphoid hyperplasias (lymphadenopathies)

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
Generic image for table
Table 17.2

Morphologic classification of non-Hodgkin's lymphomas a

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
Generic image for table
Table 17.3

Characterization of B-cell tumors a

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
Generic image for table
Table 17.4

Correlation between histiocytic grade and Ki-67 positivity

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
Generic image for table
Table 17.5

Characterization of T-cell tumors a

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
Generic image for table
Table 17.6

Classification of macrophage-histiocyte-derived tumors

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
Generic image for table
Table 17.7

Histopathologic classification of Hodgkin's disease a

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17
Generic image for table
Table 17.8

Some gene rearrangements in human malignant lymphomas and leukemias

Citation: Sell S. 2001. Immunoproliferative Diseases, p 528-555. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch17

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