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Color Plates

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Figures

Image of Color Plate 1 (chapter 1).

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Color Plate 1 (chapter 1).

(A) Electron micrograph of an A/E lesion caused by EPEC. (B) Model of protein secretion and Tir-intimin binding. The LEE-encoded Esc proteins form the secretion apparatus, and EspA-containing filaments form a channel through which secreted proteins are translocated into the host cytosol. EspB and EspD are thought to form a translocation pore in the host plasma membrane. Tir is one effector protein translocated into the host, where it is phosphorylated on tyrosine. It is then inserted into the plasma and serves as the receptor for the EPEC outer membrane protein, intimin, through its extracellular intimin binding domain (IBD). The Tir-intimin interaction triggers pedestal formation and A/E lesion induction. Electron micrograph courtesy of F. Ebel, Institut Pasteur, Paris, France. Model reproduced from Celli et al. (2000) with permission.

Citation: Kaufmann S, Sher A, Ahmed R. 2002. Color Plates, In Immunology of Infectious Diseases. ASM Press, Washington, DC.
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Image of Color Plate 2 (chapter 1).

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Color Plate 2 (chapter 1).

Model of cytoskeletal changes induced by . . Following contact with the host cell, the Ipa proteins IpaB and IpaC are inserted into the host plasma membrane by the type III secretion apparatus. These proteins form a pore through which IpaA is secreted into the host cytosol. IpaA interacts with vinculin, resulting in its unfolding and thus mediating the interaction between vinculin and actin. IpaC can activate the small GTPases Cdc42 and Rac, whereas Rho is activated by Rac. These changes culminate in the actin rearrangements that are required to form the macropinocytotic structure that mediates entry. Model courtesy of R. Bourdet-Sicard, Institut Pasteur, Paris, France.

Citation: Kaufmann S, Sher A, Ahmed R. 2002. Color Plates, In Immunology of Infectious Diseases. ASM Press, Washington, DC.
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Image of Color Plate 3 (chapter 7).

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Color Plate 3 (chapter 7).

Signaling pathways of innate immunity in cells and in mammalian cells. On the left are the pathways involved in the induction of the antifungal gene drosomycin when the processed Spaetzle protein binds to Toll. On the right are similar pathways that take place in mammalian cells when the bacterial product LPS interacts with TLR4, leading to activation of costimulatory genes. DD, death domains; KD, kinase domain; LRR, leucine-rich repeat domain. For details, see Hoffman et al. (1999) and Medzhitov et al. (1997). Reproduced from Hoffman et al. (1999) with permission of the American Association for the Advancement of Science.

Citation: Kaufmann S, Sher A, Ahmed R. 2002. Color Plates, In Immunology of Infectious Diseases. ASM Press, Washington, DC.
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Image of Color Plate 4 (chapter 14).

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Color Plate 4 (chapter 14).

Inductive and effector sites in mucosal tissues. Different strategies are used to sample antigens across epithelial barriers and deliver them to inductive sites. In stratified epithelia (oral cavity and vagina), circulating monocytes are recruited that differentiate within the epithelial microenvironment into Langerhans’ cells or DCs. These cells capture and internalize antigenic macromolecules and microorganisms and subsequently migrate into local MALT or, via lymphatics, into the draining lymph nodes. In simple epithelia, M cells transport antigens into MALT, where they are taken up by DCs. If induction of the immune response occurs in MALT and lymph nodes associated with mucosal tissues, the effector and memory immune cells acquire a mucosal homing program (αβ integrin) and return to mucosal effector sites. If induction occurs in distant organized lymphoid tissues, the resulting effector and memory cells express a systemic homing program.

Citation: Kaufmann S, Sher A, Ahmed R. 2002. Color Plates, In Immunology of Infectious Diseases. ASM Press, Washington, DC.
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Image of Color Plate 5 (chapter 22).

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Color Plate 5 (chapter 22).

(Row 1, left) SIV in a naturally infected sooty mangabey. In situ hybridization for viral RNA shows an infected lymphocyte in the lamina propria of the jejunum. Nitroblue tetrazolium—5-bromo-4-chloro-3-indolyl phosphate chromogen (blue) with nuclear fast red counterstain. Magnification, ×368. (Row 1, middle) Influenza A virus infection in the lung of a human. Viral antigens are present in lining bronchial epithelial cells. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, ×46. (Row 1, right) Rotavirus infection in the small intestine of a human. Viral antigens are present in superficial epithelial cells of small intestine and cellular debris. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, ×92. (Row 2, left) Dengue virus infection in the spleen of a human. Viral antigens are present in endothelial cells of a large vessel. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, ×145. (Row 2, middle) Dengue virus infection in the liver of a human. Viral antigens are present in Kupffer cells and sinusoidal lining cells of the liver. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, ×145. (Row 2, right) Rift Valley fever virus infection in the liver of a human. Viral antigens are present in hepatocytes, Kupffer cells, and sinusoidal lining cells of the liver. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, ×92. (Row 3, left) Eastern equine encephalitis virus infection in the brain of a human. Most cells were infected, as evidenced by the presence of viral antigens in neurons and neuronal processes. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, ×46. (Row 3, middle) Nipah virus infection in the brain of a human. Viral antigens are present in neurons and neuronal processes. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, ×46. (Row 3, right) West Nile virus infection in the brain of a human. Viral antigens are present in neurons and neuronal processes. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, ×46. (Row 4, left) Adenovirus infection in the brain of a human. Viral antigens are present in neurons and neuronal processes. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, ×145. (Row 4, middle) Measles virus infection in the lung of a human. Multinucleated syncytial cells (arrows) are seen in the bronchial epithelium. Hematoxylin and eosin stain. Magnification, ×145. (Row 4, right) Measles virus infection in the lung of a human. Viral antigens are present in intranuclear inclusions of multinucleated syncytial cells. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, ×145.

Citation: Kaufmann S, Sher A, Ahmed R. 2002. Color Plates, In Immunology of Infectious Diseases. ASM Press, Washington, DC.
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Image of Color Plate 6 (chapter 22).

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Color Plate 6 (chapter 22).

(Row 1, left) Nipah virus infection in the lung of a pig. Viral antigens are present in bronchial epithelial cells and sloughing cellular debris. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, ×145. (Row 1, middle) Respiratory syncytial virus infection in the lung of a human. Viral antigens are present in the nuclei and cytoplasm of multinucleated syncytial cells. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, ×46. (Row 1, right) BK polyomavirus infection in the urinary bladder of a human. Multiple viral inclusions (arrows) are present in epithelial cells. Hematoxylin and eosin stain. Magnification, ×145. (Row 2, left) BK polyomavirus infection in the urinary bladder of a human. Viral antigens are present in epithelial cells. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, ×92. (Row 2, middle) Nipah virus infection in the urinary bladder of a pig. Viral antigens are present in epithelial cells and multinucleated syncytial cells. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, 92. (Row 2, middle) Nipah virus infection in the urinary bladder of a pig.92. (Row 2, right) Adenovirus infection in the lung of a human. Viral inclusions and smudge cells are present in the interstitium and alveolar space. Hematoxylin and eosin stain. Magnification, 92. (Row 2, middle) Nipah virus infection in the urinary bladder of a pig.230. (Row 3, left) Varicella-zoster virus infection in the skin of a human. Large intranuclear inclusions (arrows) are present in the epidermis. Hematoxylin and eosin stain. Magnification, 92. (Row 2, middle) Nipah virus infection in the urinary bladder of a pig.145. (Row 3, middle) Rabies virus infection in the cerebellum of a human. An intracytoplasmic inclusion body (Negri body [arrow]) is present in a Purkinje cell. Hematoxylin and eosin stain. Magnification, 92. (Row 2, middle) Nipah virus infection in the urinary bladder of a pig.145. (Row 3, right) Human parvovirus infection in the bone marrow of a human. Intranuclear inclusions (arrows) are present in nucleated red blood cells. Hematoxylin and eosin stain. Magnification, 92. (Row 2, middle) Nipah virus infection in the urinary bladder of a pig.230. (Row 4, left) Human parvovirus infection in the bone marrow of a human. Viral antigens are present in nucleated red blood cells. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, 92. (Row 2, middle) Nipah virus infection in the urinary bladder of a pig.92. (Row 4, middle) Measles virus infection in the brain of a human with subacute sclerosing panencephalitis. Viral antigens are present in intranuclear inclusions in neurons. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, 92. (Row 2, middle) Nipah virus infection in the urinary bladder of a pig.145. (Row 4, right) Human papillomavirus infection in the cervix of a human with cervical papillary adenocarcinoma. Hematoxylin and eosin stain. Magnification, 92. (Row 2, middle) Nipah virus infection in the urinary bladder of a pig.92.

Citation: Kaufmann S, Sher A, Ahmed R. 2002. Color Plates, In Immunology of Infectious Diseases. ASM Press, Washington, DC.
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Image of Color Plate 7 (chapter 22).

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Color Plate 7 (chapter 22).

(Row 1, left) Human papillomavirus infection in the cervix of a human showing an integrated HPV genome (arrows) in carcinoma cells. In situ hybridization. Magnification, 92. (Row 2, middle) Nipah virus infection in the urinary bladder of a pig.92. (Row 1, middle) Nipah virus infection in the brain of a human. Viral antigens are present in endothelial cells and syncytial cells of cerebral vasculature. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, 92. (Row 2, middle) Nipah virus infection in the urinary bladder of a pig.145. (Row 1, right) SIV infection in the brain of a pig-tailed macaque monkey. In situ hybridization for viral RNA, showing an infected perivascular multinucleated giant cell within the parenchyma of the brain. Nitroblue tetrazolium—5-bromo-4-chloro-3-indolyl phosphate chromogen (blue) with nuclear fast red counterstain. Magnification, 92. (Row 2, middle) Nipah virus infection in the urinary bladder of a pig.368. (Row 2, left) West Nile virus infection in the brain of a human. Perivascular “cuffs” of inflammatory cells, as shown here, are a common feature of viral encephalitides and are not specific for a particular viral agent. Hematoxylin and eosin stain. Magnification, 92. (Row 2, middle) Nipah virus infection in the urinary bladder of a pig.92. (Row 2, middle) Japanese encephalitis virus infection in the brain of a human. Neuronal necrosis, neuronophagia, and parenchymal inflammation are major histopathologic features. Hematoxylin and eosin stain. Magnification, ×92. (Row 2, right) Ebola virus infection in the liver of a human. This section shows severe hepatocellular necrosis and multiple inclusions (arrows) in hepatocytes. Hematoxylin and eosin stain. Magnification, ×145. (Row 3, left) Ebola virus infection in the liver of a human. Viral antigens are present in hepatocytes, Kupffer cells, and the cells lining the hepatic sinusoids. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, ×92. (Row 3, middle) Lassa fever virus infection in the liver of a human. Viral antigens are present in hepatocytes, Kupffer cells, and cells lining the hepatic sinusoids. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, ×145. (Row 3, right) Hantavirus infection in the lung of a human. Pulmonary edema and hyaline membrane formation are present. Hematoxylin and eosin stain. Magnification, ×46. (Row 4, left) Hantavirus infection in the lung of a human. Viral antigens are present in endothelial cells of the pulmonary microvasculature. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain. Magnification, ×230. (Row 4, middle) Human immunodeficiency virus type 1 (HIV-1) infection in a chimpanzee. Immunohistochemistry for the major viral capsid antigen, p24, in a section of lymph node is shown. Note the reticular pattern of intercellular p24 reactivity within the germinal center, typical of dendritic cell trapping of virions. Immunoperoxidase reaction, with diaminobenzidine chromogen (brown) and hematoxylin counterstain. Magnification, ×368. (Row 4, right) SIV infection in the brain of a pig-tailed macaque. Most of the productively infected cells in the brain are macrophages, as revealed by the dual-label technique, using in situ hybridization to localize viral RNA (blue) and immunohistochemistry to localize the macrophage phenotype marker, Ham-56 (black). Nitroblue tetrazolium–5-bromo-4-chloro-3-indolyl phosphate chromogen (ISH) plus immunogold (IHC); counterstain was omitted. Magnification, ×368.

Citation: Kaufmann S, Sher A, Ahmed R. 2002. Color Plates, In Immunology of Infectious Diseases. ASM Press, Washington, DC.
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Image of Color Plate 8 (chapter 25).

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Color Plate 8 (chapter 25).

VSG coat of African trypanosomes. An electron photomicrograph of () LouTat 1 reveals the dense molecular packing of VSG molecules on the plasma membrane. Also shown is a structural model of the LouTat 1 VSG homodimer in an orientation that it assumes on the membrane with other identical homodimers to form the surface coat.

Citation: Kaufmann S, Sher A, Ahmed R. 2002. Color Plates, In Immunology of Infectious Diseases. ASM Press, Washington, DC.
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Image of Color Plate 9 (chapter 25).

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Color Plate 9 (chapter 25).

-induced macrophage signaling alteration. Binding of to host cell receptors is potentially responsible for the induction of deactivating events involving proteasome and SHP-1 activation. SHP-1 negatively affects JAK2 kinase and Erk1/Erk2 mitogen-activated protein kinase (MAP K) conducting to the inhibition of IFNγ-inducible macrophage functions. Proteolysis of signaling molecules such as STAT1 contributes to this inactivation process. Other phosphatases (e.g., IP3 phosphatase and calcineurin) and surface parasite molecules (i.e., LPG) are recognized for their role in the alteration of various second messengers (i.e., PKC, Ca, inositol lipids, and inositol phosphates) necessary for the induction of important phagocyte functions in response to chemotactic peptide (f-Met-Leu-Phe) and phorbol ester (PMA).

Citation: Kaufmann S, Sher A, Ahmed R. 2002. Color Plates, In Immunology of Infectious Diseases. ASM Press, Washington, DC.
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Image of Color Plate 10 (chapter 25).

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Color Plate 10 (chapter 25).

Ca homeostasis and infection. (A) Macrophage Ca mobilization induced by . and its surface molecule LPG (PG + CORE-PI; LPG structural components). (B) Thapsigargin-mediated intracellular Ca stores emptying in uninfected and . -infected cells. Reduced levels of Ca released from intracellular stores in -infected cells suggests partial Ca store depletion which could contribute to the activation of the capacitative mechanism responsible for the sustained Ca influx. (C) -induced Ca mobilization observed by confocal microscopy.

Citation: Kaufmann S, Sher A, Ahmed R. 2002. Color Plates, In Immunology of Infectious Diseases. ASM Press, Washington, DC.
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Image of Color Plate 11 (chapter 25).

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Color Plate 11 (chapter 25).

Proteasome (26S) and immunoproteasome formation. Both types of proteasomes originate from the cylindrical 20S proteasome. The 26S proteasome is involved in the proteolysis of diverse proteins, which require ubiquitination for their recognition and degradation. IFN-γ-inducible immunoproteasome is formed by the addition of immunoproteasome (LMP-2, LMP-7, and MECL-1) and catalytic (PA28α and PA28β) subunits to the 20S proteasome. Immunoproteasome is necessary for the generation of peptides to be presented in an MHC class I context. Infection of macrophages by . and . parasites leads to abnormal immunoproteasome formation.

Citation: Kaufmann S, Sher A, Ahmed R. 2002. Color Plates, In Immunology of Infectious Diseases. ASM Press, Washington, DC.
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