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Chapter 1 : Overview of Immunity

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Abstract:

The principal function of the immune system is to protect against infection. The modern appreciation of the physiologic function of the immune system is barely more than 100 years old. Blood is an important component of the immune system. It contains the hematopoietic cells, proteins, and liquid that circulates throughout the body. The major protein found in the blood and on mucosal surfaces, such as the respiratory, gastrointestinal, and urogenital tracts, that mediates immune system function is antibody. Two broad categories of immune system function have been defined: innate immunity and adaptive immunity. Phagocytic cells recognize foreign microorganisms and ingest (or engulf) them. The cell releases into the phagosome toxic compounds that digest and kill the microorganism. Polymorphonuclear neutrophils (PMNs) are principally found in the blood and live only 12 to 24 hours. Therefore, a prodigious amount of new PMNs are made each day by an individual. However, early after an antigenic stimulus is detected, the PMNs leave the blood and travel to the site of infection, ready to ingest antigens and kill those that are living. Adaptive immunity can be subdivided into cell-mediated and humoral immunity labels that can be somewhat confusing, since both types of immunity involve cells—the lymphocytes. It is important that the immune effector mechanisms that are operative during hypersensitive responses are identical to the mechanisms that occur during appropriate and protective immune responses in other circumstances.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1

Key Concept Ranking

Immune System Proteins
1.0852585
Complement System
0.67495894
Innate Immune System
0.5992848
Adaptive Immune System
0.5960807
1.0852585
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Figures

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Figure 1.1

Organs and tissues of the immune system.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Image of Figure 1.2
Figure 1.2

Components of blood and their immune functions. The hematopoietic cells are divided into myeloid, lymphoid, and erythroid lineages. These classifications are based both on developmental events and on specific functions of the mature effector cells. Each type of hematopoietic cell serves a distinct immune function(s). There is some overlap in the functions of different cell types. The noncellular components of blood are proteins that also serve immune functions. ADCC, antibody-dependent cell-mediated cytotoxicity.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Figure 1.3

Phagocytosis. The phagocytic cell adheres to a microorganism by extrusions of the cell membrane called . The cell surrounds the microorganism and engulfs, or ingests, it into a subcellular structure called the phagosome. Other membrane-bound organelles, called contain enzymes and cytotoxic chemicals. The lysosome fuses with the phagosome and releases its contents. The engulfed microorganism is digested, and the debris is released from the cell by fusion of the phagosome to the cell membrane.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Figure 1.4

The inflammatory response. The black arrows show the path of the monocyte from its initial location in the blood circulation to its final destination at the site of injury or infection.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Figure 1.5

Effectors of the acquired immune response. The lymphocytes (T cells and B cells) are the mediators of acquired immune responses. T cells express the TCR, coreceptors (CD4 or CD8), and other cell surface proteins (CD3, Thy1). Activated T cells produce cellmediated acquired immune responses (either cytotoxic or helper functions, depending on the type of T cell stimulated). B cells express mIg or BCR and other cell surface proteins with immune functions (Ig-α/β, B220). Activated B cells produce humoral acquired immune responses (production of antibodies).

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Figure 1.6

The acquired immune response involves the activation of lymphocytes upon their encounter with specific antigen. Before encountering its antigen, the lymphocyte (then referred to as a naive lymphocyte) is quiescent. Upon encountering antigen, the lymphocyte undergoes a two-step activation process that first involves rapid cell division (proliferation) and then differentiation into a mature cell type. Each activated lymphocyte that results from the period of proliferation differentiates into either an effector cell (which can carry out immune functions) or a memory cell. The memory cell reenters a resting state to await encounter with the same antigen.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Figure 1.7

Generation of TCRs by gene rearrangement. The gene that eventually encodes the TCR originally consists of many . Some of these gene segments, called and segments, are randomly combined with each other to produce a combination of segments that confers a unique antigenic specificity on the TCR (due to the variable region). Another portion of the TCR gene (called the constant region) is not altered by the gene rearrangements. This portion of the TCR gene is the same for all TCRs in each of the four TCR classes (α, β, γ, and δ).

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Figure 1.9

Simplified view of antigen presentation. A microorganism (in this case, a bacterium) is phagocytosed and killed by an APC. The green and red circles represent hydrolytic enzymes that are stored in vesicles known as lysosomes. Portions of the digested bacterium are displayed on the surface of the phagocytic cell by MHC proteins The TCR recognizes the antigen, and the coreceptor recognizes the MHC.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Figure 1.8

Simplified view of antigen recognition by a T cell. The T cell recognizes not a whole, intact antigen, but a small peptide fragment of a protein antigen complexed to an MHC protein. For the T cell to become activated, its antigen receptor must be able to recognize both the MHC and the antigenic peptide.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Image of Figure 1.10
Figure 1.10

Interactions between a helper or cytotoxic T cell and an APC. TH cells express the CD4 coreceptor, which interacts with MHC class II on a professional APC. TH cells enhance the functions of other immune cells (phagocytic or B cells). Cytotoxic T cells express the CD8 coreceptor, which interacts with MHC class I on any cell (called a target cell). Cytotoxic T cells lyse target cells presenting the antigen (Ag) for which the T cell is specific.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Image of Figure 1.11
Figure 1.11

Structural diagram of an antibody. Antibodies are tetramers consisting of four peptides: two heavy chains and two light chains. Both the heavy and light chains have constant regions (blue), where the amino acid sequence is conserved (similar) among all antibodies, and variable regions (green), where the amino acid sequence is unique to that particular antibody. Antibodies may be secreted or may be “tethered” to the cell surface by a short, transmembrane domain added to the amino acid sequence of the heavy chain.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Figure 1.12

Activation of B cells. For most antigens, activation of B cells requires two signals. Signal 1 is delivered by the binding of the antigen to the mIg on the B cell. Signal 2 is delivered to the B cell by a TH cell that is also stimulated by antigenic fragments bound to MHC molecules. Activation of a B cell in this manner leads to differentiation of the B cell into an antibody (Ig)-secreting plasma cell. This figure also highlights the fact that B cells and T cells recognize the same antigen by two different mechanisms—the B cell by “directly” binding to the intact antigen and the T cell by recognizing a peptide fragment of the antigen complexed to an MHC protein.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Figure 1.13

T-cell-independent antigens. Type 1 T-cellindependent antigens (TI-1 Ag) are mitogenic for B cells, regardless of the antigenic specificities of the B cell. Type 2 T-cell-independent antigens (TI-2 Ag) engage many BCRs of the same specificity on a single B-cell surface at the same time, effectively cross-linking the mIg and activating the B cell in a manner that does not depend on activational signals from a TH cell.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Image of Figure 1.14
Figure 1.14

Sequence of innate and acquired events in an immune response. Typically, innate responses are immediate and are followed by acquired responses. The acquired immune responses, however, can regulate innate responses and vice versa.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Image of Figure 1.15
Figure 1.15

Example of innate responses regulating innate and acquired mechanisms. Activated () complement can interact with macrophages or neutrophils to enhance phagocytic killing or with NK cells to enhance cytotoxicity. This is possible because macrophages, neutrophils, and NK cells possess cell surface receptors (CR3 and CR4) for activated complement.While this enhances the innate immune response in neutrophils and NK cells, it also affects the acquired immune response, since the enhancement of phagocytosis by macrophages leads to higher levels of antigen presentation to T cells.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Image of Figure 1.16
Figure 1.16

Example of acquired response influencing innate mechanisms. The cytokines produced by cells of the acquired immune response (mostly TH cells) influence activation of cells of the innate immune response, such as macrophages, neutrophils, eosinophils, and NK cells. Several particular cytokines are named as examples: MCF, macrophage chemotactic factor; MIF, migration inhibitory factor; IFN-γ, interferongamma; TNF-β, tumor necrosis factor beta; IL, interleukin.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Figure 1.17

Examples of antibody-mediated effector mechanisms that combat bacterial infection. Gram-negative bacteria are susceptible to a number of effector mechanisms. Antibody can trigger complement activation, leading to the formation of a MAC on the bacterium’s outer membrane. In addition, both antibody and complement proteins that bind to the bacterium can target the bacterium for macrophages and neutrophils, which express antibody Fc receptors (FcR) and complement receptors (CR). These cells can kill the bacterium through either phagocytosis or the release of toxic mediators (ADCC). Gram-positive bacteria have no outer membrane and are therefore not susceptible to MAC formation. However, they are still susceptible to opsonization and ADCC after antibody binding and/or complement activation.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Figure 1.18

Examples of antibody-mediated effector mechanisms that combat viral infection. Enveloped viruses are susceptible to MACs and antibody- and complement-mediated opsonization for phagocytosis by macrophages and neutrophils, which express antibody Fc receptors (FcR) and complement receptors (CR). Nonenveloped viruses have no membrane and are therefore not susceptible to MAC formation. However, they are still susceptible to opsonization after antibody binding and/or complement activation In addition, antibodies and activated complement proteins can enshroud a virus in a thick layer of protein Although this does not kill the virus, it can render it noninfectious.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Image of Figure 1.19
Figure 1.19

NK cells are able to kill host cells that exhibit abnormal expression of MHC class I proteins. If a target cell expresses normal levels of MHC class I an inhibitory receptor on the NK cell binds the MHC and prevents the NK cell from killing the target. If the target cell expresses reduced amounts of MHC class I the inhibitory receptor does not deliver this inhibitory signal and the NK cell kills the target cell. Some tumors demonstrate reduced expression of MHC class I and are thus poorly recognized by CTLs. This reduced expression of MHC class I may allow NK cells to kill the tumor cell. Therefore, NK cells can function as a “backup” killing mechanism.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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Figure 1.20

Antibody-mediated hypersensitive reactions occur by different mechanisms, depending in part on which isotype of antibody is produced. IgE antibodies mediate immediate-type hypersensitivity by binding to Fc receptors on the surface of mast cells. Subsequent binding of this IgE by an antigen (called an allergen) results in mast cell activation and the release of compounds such as histamine that cause the allergic response. IgG antibodies can cause a form of hypersensitivity brought about by destruction of a normal host cell by complement activation, phagocytosis, or ADCC. The example shown depicts antibody-mediated hemolysis of a red blood cell (RBC) such as might occur after transfusion of incompatible blood into a patient. IgG antibodies can also cause hypersensitivity if they form immune complexes with antigen that become immobilized or lodged in tissues such as vascular beds. In this case, localized complement activation draws neutrophils to the site that bind the immune complexes and release toxic substances such as proteases, glycosidases, and reactive oxygen intermediates (ROIs), causing to the nearby tissues.

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
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References

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1. Delves, P. J., , and I. M. Roitt . 2000 . The immune system. Part I . N. Engl. J. Med. 343:3749.
2. Delves, P. J., , and I. M. Roitt . 2000 . The immune system. Part II . N. Engl. J. Med. 343:108117.
3. Foss, F. M. 2002 . Immunologic mechanisms of antitumor activity . Semin. Oncol. 29(3 Suppl. 7):511.
4. Leng, Q., , and Z. Bentwich . 2002 . Beyond self and nonself: fuzzy recognition of the immune system . Scand. J. Immunol. 56: 224232.
5. Maddox, L., , and D. A. Schwartz . 2002 . The pathophysiology of asthma . Annu. Rev. Med. 53:477498.
6. Medzhitov, R., , and C. Janeway, Jr. 2000 . Innate immunity . N. Engl. J. Med. 343:338344.
7. Rotrosen, D., , J. B. Matthews, , and J. A. Bluestone . 2002 . The immune tolerance network: a new paradigm for developing tolerance- inducing therapies . J. Allergy Clin. Immunol. 110:1723.
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Tables

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Table 1.1

Types of immunity

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
Generic image for table
Table 1.2

Mechanisms of innate immunity

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
Generic image for table
Table 1.3

Lymphocytes and proteins involved in acquired immune response

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1
Generic image for table
Table 1.4

Immunoglobulin classes

Citation: Yates K, Lyczak J. 2004. Overview of Immunity, p 3-28. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch1

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