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18 Interaction of Pathogens with the Innate and Adaptive Immune System

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18 Interaction of Pathogens with the Innate and Adaptive Immune System, Page 1 of 2

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Abstract:

The host response to pathogenic microorganisms is extraordinarily diverse. The extent and degree of the host response depend on the nature of the pathogen itself and the route and extent of the infection. Some general features of host-pathogen interactions are discussed in this chapter. Probably the best experimental approach to the analysis of the innate response is to examine mutant mice that can use only the innate system, by virtue of the absence of lymphocytes. The activated macrophage is found as a result of activation of either the innate immune system or the T-cell system. The innate system is activated when macrophages interact with microbes and release early cytokines that induce natural killer (NK) cells to produce interferon (IFN)-γ. Neutrophils are essential in infections with extracellular bacteria, which are rapidly eliminated by the oxidative and nonoxidative neutrophil microbicidal mechanisms. The most extensively studied infection that has led to insights into the activation of the innate immune system is infection in the SCID mouse. The peptide-major histocompatibility complex (MHC) molecular complex represents the molecular substrate that engages the T-cell receptor (TCR) for antigen. The composition of the peptide-MHC complex reflects the intracellular milieu of the antigen-presenting cells (APC).

Citation: Unanue E, De Gregorio E. 2004. 18 Interaction of Pathogens with the Innate and Adaptive Immune System, p 425-449. In Cossart P, Boquet P, Normark S, Rappuoli R (ed), Cellular Microbiology, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817633.ch18

Key Concept Ranking

Innate Immune System
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Adaptive Immune System
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Figures

Image of Figure 18.1
Figure 18.1

Dynamics of infection in normal and SCID mice. In normal mice there is exponential growth and the infection is controlled. The cells involved at different stages are indicated. In SCID mice, the absence of lymphocytes results in persistence of the infection. The early components of the infection involve neutrophils and NK cells, while lymphocytes are essential for clearance of the infection.

Citation: Unanue E, De Gregorio E. 2004. 18 Interaction of Pathogens with the Innate and Adaptive Immune System, p 425-449. In Cossart P, Boquet P, Normark S, Rappuoli R (ed), Cellular Microbiology, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817633.ch18
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Image of Figure 18.2
Figure 18.2

General features of a class I MHC molecule. The α and α domains create the peptide-binding site, which is on top of the molecule. The α domain is an Ig-like domain. A small polypeptide, β-microglobulin, forms part of the complex. (In the class II MHC molecule, the combining site is formed by the two most external domains of the α and β chains, which make up a structure similar to the combining site of class I molecules.)

Citation: Unanue E, De Gregorio E. 2004. 18 Interaction of Pathogens with the Innate and Adaptive Immune System, p 425-449. In Cossart P, Boquet P, Normark S, Rappuoli R (ed), Cellular Microbiology, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817633.ch18
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Image of Figure 18.3
Figure 18.3

Structure of a peptide bound to the combining site of a class II MHC molecule. This specific example shows a lysozyme peptide bound to the murine molecule. The peptide is stretched out and slightly twisted. The TCR contacts some of the solvent-exposed residues as well as the helices of the α (top) and β (below) domains. Adapted from D. H. Fremont, D. Monnaie, C. A. Nelson, W. A. Hendrickson, and E. R. Unanue, 305, 1998.

Citation: Unanue E, De Gregorio E. 2004. 18 Interaction of Pathogens with the Innate and Adaptive Immune System, p 425-449. In Cossart P, Boquet P, Normark S, Rappuoli R (ed), Cellular Microbiology, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817633.ch18
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Image of Figure 18.4
Figure 18.4

Regulation of CD4 T-cell differentiation. Reprinted from A. O'Garra, 275–283, 1998.

Citation: Unanue E, De Gregorio E. 2004. 18 Interaction of Pathogens with the Innate and Adaptive Immune System, p 425-449. In Cossart P, Boquet P, Normark S, Rappuoli R (ed), Cellular Microbiology, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817633.ch18
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Image of Figure 18.5
Figure 18.5

Pathogen-activated innate immune pathways in and mammalian cells. In (left panel) gram-positive bacteria are recognized by two PRRs, PGRP-SA and GNBP1, which trigger the activation of a proteolytic cascade that activates Spaetzle. A cleaved form of Spaetzle directly activates Toll. The signal is transmitted through a homologue of MyD88 (DMyD88) and an IRAK-like protein kinase (Pelle), leading to phosphorylation of the IκB-homologue Cactus, the nuclear translocation of the NF-κB homologues Dif and Dorsal and the activation of immune-responsive genes, including antimicrobial peptide genes. In mammals (right panel) PAMPs associated with various extracellular pathogens elicit the activation of TLRs, which can transmit the signal through two TIR containing proteins: MyD88, which activates NF-κB and MAPK pathways leading to up-regulation of several immune responsive genes including proinflammatory cytokines and costimulatory molecules, and TRIF, triggering the IRF-3/interferon β response. Peptidoglycan (PG) associated with intracellular bacteria is recognized by NOD1 and 2, which activate NF-κB pathway through RICK. Abbreviations: PAMPs, pathogen-associated molecular patterns; TLRs, Toll-like receptors; LRR, leucinerich repeat domain; TIR, Toll-IL1 receptor domain; DD, death domain; CARD, caspase activation and recruitment domain; RHD, Rel homology domain; ANK, ankyrin repeats domain; K, kinase domain; IRAK, IL1-receptor-associated kinase; TRAF, TNF-receptor-associated kinase; NF-κB: nuclear factor κB; IκB, inhibitor of κB; IKK: IκB kinase; MAPK, mitogen-activated protein kinase; IFN, interferon; PGRP, peptidoglycan recognition protein; GNBP, gram-negative binding protein.

Citation: Unanue E, De Gregorio E. 2004. 18 Interaction of Pathogens with the Innate and Adaptive Immune System, p 425-449. In Cossart P, Boquet P, Normark S, Rappuoli R (ed), Cellular Microbiology, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817633.ch18
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References

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Tables

Generic image for table
Table 18.1

Properties of macrophages

Citation: Unanue E, De Gregorio E. 2004. 18 Interaction of Pathogens with the Innate and Adaptive Immune System, p 425-449. In Cossart P, Boquet P, Normark S, Rappuoli R (ed), Cellular Microbiology, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817633.ch18
Generic image for table
Table 18.2

Generation of activated macrophages

Citation: Unanue E, De Gregorio E. 2004. 18 Interaction of Pathogens with the Innate and Adaptive Immune System, p 425-449. In Cossart P, Boquet P, Normark S, Rappuoli R (ed), Cellular Microbiology, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817633.ch18
Generic image for table
Table 18.3

Properties of SCID mice

Citation: Unanue E, De Gregorio E. 2004. 18 Interaction of Pathogens with the Innate and Adaptive Immune System, p 425-449. In Cossart P, Boquet P, Normark S, Rappuoli R (ed), Cellular Microbiology, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817633.ch18
Generic image for table
Table 18.4

Properties of class I and II MHC molecules

Citation: Unanue E, De Gregorio E. 2004. 18 Interaction of Pathogens with the Innate and Adaptive Immune System, p 425-449. In Cossart P, Boquet P, Normark S, Rappuoli R (ed), Cellular Microbiology, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817633.ch18
Generic image for table
Table 18.5

Experimental manipulations that influence resistance to in the mouse

Citation: Unanue E, De Gregorio E. 2004. 18 Interaction of Pathogens with the Innate and Adaptive Immune System, p 425-449. In Cossart P, Boquet P, Normark S, Rappuoli R (ed), Cellular Microbiology, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817633.ch18
Generic image for table
Table 18.6

PAMPs from various microorganisms that elicit mammalian Toll-like receptors

Citation: Unanue E, De Gregorio E. 2004. 18 Interaction of Pathogens with the Innate and Adaptive Immune System, p 425-449. In Cossart P, Boquet P, Normark S, Rappuoli R (ed), Cellular Microbiology, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817633.ch18

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