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Chapter 15 : Interplay of Inflammatory and Immunopathologic Mechanisms, Immune Defense, and Evasion of Immune Defense Mechanisms during Infection

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Interplay of Inflammatory and Immunopathologic Mechanisms, Immune Defense, and Evasion of Immune Defense Mechanisms during Infection, Page 1 of 2

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Abstract:

In any inflammatory reaction, both immune and "nonimmune" mechanisms may be activated. Inflammation may be activated by nonimmune factors such as tissue necrosis (infarct), release of bacterial products, or trauma. In most cases, nonimmune inflammatory reactions or the clotting system are activated secondary to tissue damage caused by immunopathologic mechanisms, and successful treatment may be directed to both the primary immunopathologic process and the secondary inflammatory process. The interactions of various immune effector mechanisms are seen in infectious diseases in roles of protection and pathogenesis. Many other infectious diseases have similar, if not so complicated, mixtures of immunoprotective and immunopathologic mechanisms. The many different immune effector mechanisms have most likely evolved as a means for defending us against many different infectious agents. In return, infectious organisms have evolved many “ingenious” ways to avoid immune defense mechanisms. Finally, in progressive disease, leishmaniae are able to modulate the T-cell immune response so that TDTH cells are not induced to activate the macrophages (immune deviation), similar to what occurs in lepromatous leprosy. The relative contribution of different immune mechanisms to the pathogenesis of other infectious diseases reflects even more variations in the interplay between immune effector mechanisms in protection and pathogenesis. The ability of many organisms to cause disease depends upon their ability to evade the immune defenses.

Citation: Sell S. 2001. Interplay of Inflammatory and Immunopathologic Mechanisms, Immune Defense, and Evasion of Immune Defense Mechanisms during Infection, p 478-509. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch15
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Figures

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Figure 15.1

Possible interactions of immune complex and other immunopathologic mechanisms. See text for description.

Citation: Sell S. 2001. Interplay of Inflammatory and Immunopathologic Mechanisms, Immune Defense, and Evasion of Immune Defense Mechanisms during Infection, p 478-509. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch15
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Figure 15.2

Antibody-mediated and cell-mediated mechanisms of protection against bacterial infections. Bacterial infections may be resisted by each of the antibody-mediated immune mechanisms, including (1) neutralization of bacterial toxins, (2) cytotoxic lysis by antibody and complement, (3) acute polymorphonuclear infiltration (Arthus reaction) and opsonization of bacteria leading to increased phagocytosis, and (4) acute anaphylactic vascular events permitting exudation of inflammatory cells and fluids. During the chronic stage of the infection, cell-mediated immunity is activated: (5) TCTL cells that react with antigens on the surface of virus-infected cells and cause their destruction. (6) TDTH cells that react with bacterial antigens may infiltrate the site of infection, become activated, and release lymphokines that attract and activate macrophages. The activated macrophages phagocytose and degrade necrotic bacteria and tissue, preparing the lesion for healing. Granulomas form when organisms cannot be destroyed by macrophages, walling off the infection from the rest of the host.

Citation: Sell S. 2001. Interplay of Inflammatory and Immunopathologic Mechanisms, Immune Defense, and Evasion of Immune Defense Mechanisms during Infection, p 478-509. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch15
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Figure 15.3

Cellular and antibody-mediated mechanisms of protection against viral infections. Circulating immunoglobulin antibody (usually IgG) or secretory antibody (usually IgA) reacts with surface antigens on the virus and prevents the virus from attaching to cells (neutralizing antibody), thereby inhibiting spread of the infection. Sensitized TCTL cells may destroy virus-infected cells that express viral antigens associated with class I MHC molecules on the surface. TDTH cells reacting with viral antigens release lymphokines that activate macrophages to eliminate intracellular viral infections of macrophages.

Citation: Sell S. 2001. Interplay of Inflammatory and Immunopathologic Mechanisms, Immune Defense, and Evasion of Immune Defense Mechanisms during Infection, p 478-509. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch15
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Figure 15.4

The life cycle of S. stercoralis provides three routes of human infection: (1) infection by invasive filiform larvae excreted into the soil, (2) maturation of invasive filiform larvae from free-living organisms in the soil, and (3) autoinfection from filiform larvae that mature in the gastrointestinal tract of the host. Filiform larvae invade skin, enter the venous circulation, and pass to the alveolar capillaries. In the lung, the adolescent worms mature to adult male and female worms. The adult worms pass to the gastrointestinal tract, presumably by being coughed up and swallowed. The females lodge in the mucosa of the gastrointestinal tract, set up housekeeping, and lay many eggs; the male is no longer needed and most likely is passed out in the feces. In the gastrointestinal tract, eggs may mature to rhabdiform larvae and to filiform larvae. All of these forms may be passed into the soil. In addition, filiform larvae may invade the intestinal mucosa, particularly at the anal canal, permitting autoinfection.

Citation: Sell S. 2001. Interplay of Inflammatory and Immunopathologic Mechanisms, Immune Defense, and Evasion of Immune Defense Mechanisms during Infection, p 478-509. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch15
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Figure 15.5

Antigenic variation during trypanosomiasis infection. Successive waves of different clones expressing different surface glycoproteins (VSG, variable surface glycoproteins) of the parasite are characteristic of trypanosomiasis. After infection, one clone of parasites, most of which carry a particular VSG, proliferates in the bloodstream. Antibody is produced to this VSG and kills most of the parasites. A few individuals survive by expressing a new VSG. This clone then expands until antibody to the new VSG is produced and kills most of the second wave. This process is repeated over and over again as new clones are produced. (From J. E. Donelson and M. J. Turner, Sci. Am. 252:44, 1985.)

Citation: Sell S. 2001. Interplay of Inflammatory and Immunopathologic Mechanisms, Immune Defense, and Evasion of Immune Defense Mechanisms during Infection, p 478-509. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch15
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Figure 15.6

The canyon hypothesis. This hypothesis states that the virus-binding site for a cell surface receptor for the virus is located in a depression of the viral spikes on the surface of the virus particles and that this location, while able to receive the cell surface receptor (R), sterically prevents larger antibody paratopes (P) from reacting. This allows for conservation of the virus binding site while at the same time permitting evolution of new serotypes by mutating epitopes about the rim of the canyon. (Modified from M. Luo, G. Vriend, G. Kamer, I. Minor, E. Arnold, M. G. Rossmann, U. Boege, D. G. Scraba, G. M. Duke, and A. C. Palmenberg, Science 235:182–191, 1987.)

Citation: Sell S. 2001. Interplay of Inflammatory and Immunopathologic Mechanisms, Immune Defense, and Evasion of Immune Defense Mechanisms during Infection, p 478-509. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch15
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Figure 15.7

Bipolar bridging prevents complement activation. HSV infection induces Fc receptors on the surface of infected cells that tie up the Fc domain of antibody that binds to either of the dominant antigens of HSV-1, gC or gD, through the antigen-binding site (paratope) on the Fab domain. This prevents aggregation of the Fc regions of antibodies on the surface of the cell and prevents binding of C1 of complement. (Modified from I. Frank and H. M. Friedman, J. Virol. 63:4479, 1989.)

Citation: Sell S. 2001. Interplay of Inflammatory and Immunopathologic Mechanisms, Immune Defense, and Evasion of Immune Defense Mechanisms during Infection, p 478-509. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch15
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Figure 15.8

A comparison of the association of DTH and antibody production in the clinical forms of leprosy and in the clinical stages of syphilis. The overlapping triangles indicate the relative strength of DTH and antibody production. The crosshatched triangle indicates DTH; the open triangle, antibody production. High levels of DTH are associated with cure; weak DTH is associated with progressive disease; balanced DTH and antibody production are associated with borderline leprosy and latent syphilis. Progression of syphilis to the tertiary stage is most likely more related to depressed T-cell immunity, with or without high levels of antibody. The nature of the antigen-presenting cell may determine if Th1 cells are activated to help in antibody production or in development of DTH. Antibody production is stimulated by antigens processed by dendritic follicular cells; DTH is stimulated by antigens processed by interdigitating reticulum cells.

Citation: Sell S. 2001. Interplay of Inflammatory and Immunopathologic Mechanisms, Immune Defense, and Evasion of Immune Defense Mechanisms during Infection, p 478-509. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch15
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Image of Figure 15.9
Figure 15.9

Immune evasion during L. donovani infection. (1) Motile promastigotes injected by the bite of the infected sandfly are able to activate C3 to C3b, bind to macrophages through C3b and CR1/CR3, and are endocytosed without a fatal oxygen burst. (2) Inside the cell, the promastigotes transform into amastigotes that are resistant to the oxygen-dependent and enzymatic killing process of the phagocyte. (3) Infected macrophages in T-cell zones of lymph nodes present antigens preferentially to Th2 helper cells, which release colony-stimulating inhibitory factor (CSIF), IL-3, granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-4. (4) CSIF inhibits activation of Th1 helper cells and prevents development of TDTH cells and DTH. (5) IL-3 and GM-CSF stimulate the bone marrow to produce immature monocytes, which are permissive for parasite replication. (6) IL-4 inhibits maturation of monocytes to a state of being able to resist parasite infestation.

Citation: Sell S. 2001. Interplay of Inflammatory and Immunopathologic Mechanisms, Immune Defense, and Evasion of Immune Defense Mechanisms during Infection, p 478-509. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch15
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Tables

Generic image for table
Table 15.1

Major immune defense mechanisms for infectious diseases

Citation: Sell S. 2001. Interplay of Inflammatory and Immunopathologic Mechanisms, Immune Defense, and Evasion of Immune Defense Mechanisms during Infection, p 478-509. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch15
Generic image for table
Table 15.2

Clinical manifestations of Lyme diseasea a

Citation: Sell S. 2001. Interplay of Inflammatory and Immunopathologic Mechanisms, Immune Defense, and Evasion of Immune Defense Mechanisms during Infection, p 478-509. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch15
Generic image for table
Table 15.3

Some mechanisms of evasion of immune defenses by infectious agents

Citation: Sell S. 2001. Interplay of Inflammatory and Immunopathologic Mechanisms, Immune Defense, and Evasion of Immune Defense Mechanisms during Infection, p 478-509. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch15
Generic image for table
Table 15.4

Postulated specific immune defense mechanisms in some infectious diseases

Citation: Sell S. 2001. Interplay of Inflammatory and Immunopathologic Mechanisms, Immune Defense, and Evasion of Immune Defense Mechanisms during Infection, p 478-509. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch15

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