Cell-Mediated Immune Response
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2016 Career Development Grants for Postdoctoral Women Recipients
- Publication Date : December 2016
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The ASM Membership Board is pleased to announce the recipients of the 2016 Career Development Grants for Postdoctoral Women:
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Paleomicrobiology of Human Tuberculosis
- Author: Helen D. Donoghue
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Citation: Donoghue H. 2016. Paleomicrobiology of human tuberculosis. 4(4): doi:10.1128/microbiolspec.PoH-0003-2014
- DOI 10.1128/microbiolspec.PoH-0003-2014
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Abstract:
Tuberculosis is a significant global disease today, so understanding its origins and history is important. It is primarily a lung infection and is transmitted by infectious aerosols from person to person, so a high population density encourages its spread. The causative organism is Mycobacterium tuberculosis, an obligate pathogen in the M. tuberculosis complex that also contains closely related species, such as Mycobacterium bovis, that primarily infect animals. Typical bone lesions occur in about 5% of untreated infections. These can be recognized in historical and archaeological material, along with nonspecific paleopathology such as new bone formation (periostitis), especially on ribs. Based on such lesions, tuberculosis has been found in ancient Egypt, pre-Columbian America, and Neolithic Europe. The detection of M. tuberculosis ancient DNA (aDNA) by using PCR led to the development of the new field of paleomicrobiology. As a result, a large number of tuberculosis cases were recognized in mummified tissue and bones with nonspecific or no lesions. In parallel with these developments, M. tuberculosis cell wall lipid biomarkers have detected tuberculosis suggested by paleopathology and confirmed aDNA findings. In well-preserved cases, molecular typing has identified M. tuberculosis lineages and genotypes. The current interest in targeted enrichment, shotgun sequencing, and metagenomic analysis reveals ancient mixed infections with different M. tuberculosis strains and other pathogens. Identification of M. tuberculosis lineages from samples of known age enables the date of the emergence of strains and lineages to be calculated directly rather than by making assumptions on the rate of evolutionary change.
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Enteroviruses and Parechoviruses
- Author: James J. Dunn
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Citation: Dunn J. 2016. Enteroviruses and parechoviruses. 4(3): doi:10.1128/microbiolspec.DMIH2-0006-2015
- DOI 10.1128/microbiolspec.DMIH2-0006-2015
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Abstract:
Infections with enteroviruses and human parechoviruses are highly prevalent, particularly in neonates, where they may cause substantial morbidity and mortality. Individuals with B-cell-related immunodeficiencies are at risk for severe enteroviral infections, usually a chronic and fatal meningoencephalitis. In transplant recipients and patients with malignancy, enterovirus infections typically involve the respiratory tract, but cases of severe, disseminated infection have been described. The mainstay of diagnosis for enterovirus and human parechovirus infections involves the use of molecular diagnostic techniques. However, routine nucleic acid-detection methods for enteroviruses will not detect human parechoviruses. Laboratory diagnosis of these viral infections is important in determining a patient’s prognosis and guiding clinical management.
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Salivary Histatins: Structure, Function, and Mechanisms of Antifungal Activity
- Authors: Woong Sik Jang, Mira Edgerton
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Source: Candida and Candidiasis, Second Edition , pp 185-194
Publication Date :
January 2012
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Abstract:
Immunohistochemical studies identified serous cells of the glandular acini as the cells responsible for production of salivary histatins. Histatins exhibit fungicidal activity against several Candida species, Aspergillus fumigatus, some strains of Saccharomyces cerevisiae, and Cryptococcus neoformans. Studies of levels of salivary histatins in vivo show large intersubject variation in both the concentrations of histatins and their rates of degradation. The total concentration of histatins in whole saliva is balanced between secretion of new proteins and removal of “older” proteins by degradation. Endocytosis was initially suggested as a means of histatin cellular entry based upon the observation that bafilomycin, an inhibitor of endosomal acidification, significantly decreased antifungal activity. Confocal imaging of C. albicans cells showed that some histatin 5 was localized to the vacuole but that cells containing only vacuolar histatin were viable. The cell wall of C. albicans is a thick multilayered structure of glucans, chitin, and mannoproteins that protects cells from osmotic stress and maintains structural integrity. Animal and human clinical studies to evaluate histatins as topical agents in prevention of gingivitis reported therapeutic efficacy without adverse side effects. The major requirements for effective use of salt-insensitive fungicidal peptides are selective and specific binding and uptake by candidal cells, efficacy at low concentrations that allow rapid eradication of yeast pathogens within the ionic strength of saliva, and minimal fungal resistance.
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Biomathematical Modeling of Chlamydia Infection and Disease
- Authors: Andrew P. Craig, Patrik M. Bavoil, Roger G. Rank, David P. Wilson
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Source: Intracellular Pathogens I: Chlamydiales , pp 352-379
Publication Date :
January 2012
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Abstract:
There are many areas of Chlamydia research in which biomathematical modeling has the potential to make an important contribution. In this chapter the authors begin by reviewing the mathematical models of Chlamydia that have been published. The authors then outline a system of dynamical equations that can be used as a governing framework for examining many aspects of Chlamydia infection and pathology, including their calibration to experimental data and insights gained. Later some of the more advanced and influential models are discussed in greater detail. The chapter also talks about the likely future of biomathematical modeling of Chlamydia. The field of chlamydial biomathematical modeling has been developing over the past decade and has started to make contributions to the understanding of chlamydial development, infection, and disease. Epidemiological modeling also has relevance to Chlamydia research because of the insights it can provide about vaccine development and immunity. Although the innate response is important, it is the adaptive immune response that is vital to the resolution of chlamydial infection. A major goal in Chlamydia research is to understand what causes the pathology that can arise during a Chlamydia infection in order to determine how it can be reduced or prevented. Relatively simple mathematical frameworks can be developed for exploring mechanisms and possible implications of the data. Foundational models can then be extended both mathematically and in the laboratory.
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Toxoplasma *
- Authors: James B. McAuley, Jeffery L. Jones, Kamaljit Singh
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Source: Manual of Clinical Microbiology, 10th Edition , pp 2127-2138
Publication Date :
January 2011
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Abstract:
Serologic prevalence data indicate that toxoplasmosis is one of the most common infections of humans throughout the world. Toxoplasmosis can be categorized into four groups: (i) acquired in the immunocompetent patient; (ii) acquired or reactivated in the immunodeficient patient; (iii) congenital; and (iv) ocular. Acquired infection with Toxoplasma in immunocompetent individuals is generally an asymptomatic infection. Secretions, excretions, body fluids, and tissues are potential specimens for direct observation of parasites but are generally unrewarding. The most important advantage of the immunoglobulin M (IgM) capture enzyme immunoassay (EIA) compared to indirect fluorescent antibody (IFA) is the increased detection of congenital infections: the IgM enzyme-linked immunosorbent assay (ELISA) was positive for 73% of serum samples from newborn infants with proven congenital toxoplasmosis, whereas only 25% of the same serum samples were found positive by an IFA IgM test. The currently recommended drugs work primarily against the actively dividing tachyzoite form of T. gondii and do not eradicate encysted organisms (bradyzoites). T. gondii infection is one of the most common parasitic infections worldwide and, in most instances, is of little clinical significance. The laboratory will need to use additional testing in an attempt to define the timing of infection in the case of pregnant women or the presence of actively replicating parasites in the case of the fetus, neonate, or immunosuppressed host.
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Measles and Rubella Viruses
- Authors: William J. Bellini, Joseph P. Icenogle
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Source: Manual of Clinical Microbiology, 10th Edition , pp 1372-1387
Publication Date :
January 2011
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Abstract:
This chapter combines the current laboratory diagnostic methods for measles virus and rubella virus for convenient review and reference. The measles virus genome is 15,894 nucleotides in length and contains six structural genes organized on the single strand of RNA in a gene order consistent with those of most of the paramyxoviruses, i.e., 3'-N, P. M, F, H, L-5'. A recent review by Rota et al. provides an excellent overview of the current status of the molecular epidemiology of measles and the global distribution of the various genotypes. The most common complications associated with measles virus infection are otitis media (7 to 9%), pneumonia (1 to 6%), and diarrhea (6%). Suitable samples for isolation of measles virus or for detection of viral antigen can be whole blood, serum, throat and nasopharyngeal secretions, urine, and, in special circumstances, brain and skin biopsy samples. Characteristic cytopathic effects (CPE) of measles virus infection include multinucleated cells and cellular inclusions (in-tracytoplasmic and intranuclear). The reverse transcriptase PCR (RT-PCR) should be considered for diagnostic use where IgM testing is compromised by the concurrent or recent use of measles virus-containing vaccine as part of an outbreak response or in settings of recent vaccine distribution, such as supplemental immunization activities. Groups of related viruses within the clades have been classified as genotypes. Time course of rubella virus-specific IgM and IgG detection by enzyme-linked immunosorbent assays (ELISAs) in sera of rubella patients.
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Signaling Cascades and Enzymes as Cryptococcus Virulence Factors
- Authors: Deborah S. Fox, Julianne T. Djordjevic, Tania C. Sorrell
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Source: Cryptococcus , pp 217-234
Publication Date :
January 2011
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Abstract:
Signal transduction cascades are utilized by all organisms to convey signals perceived at the cell surface to effectors within the cell. These enzymatic signaling cascades are important in the pathogenesis of many infections, including cryptococcosis. This chapter summarizes the significance and functional interactions involved in the cell wall integrity, phospholipase, and calcineurin signaling pathways for the establishment of Cryptococcus neoformans virulence. The fungal Plc enzymes referred to in this review preferentially hydrolyze phosphatidylinositol (PI)-based substrates within the cryptococcal cell and affect multiple cellular functions, including the secretion of (phospholipase B ) Plb1. It was found that the Plb1 MW could be as high as 125 kDa due to extensive asparagine N-linked glycosylation, which is responsible for at least 30% of the MW of Plb1 and essential for its activity. It was recently demonstrated that PI-PLC1 (Plc1) regulates cryptococcal virulence, acting in part through interactions with the Pkc/Mpk1 cell wall integrity pathway. In contrast to Plcs from higher eukaryotes, Plcs from the parasite Trypanosoma brucei preferentially hydrolyze the glycosylphosphatidylinositol (GPI) anchor of variant surface glycoprotein or GPI biosynthetic intermediates, in addition to PI, but not the phosphorylated intermediates, despite their localization to the peripheral cytoplasmic face of intracellular vesicles. Metabolic labeling studies performed in S. cerevisiae implicated a Plc enzyme and a secondary-acting protease in hydrolysis of the GPI anchor of certain proteins in the plasma membrane, resulting in their subsequent localization in the cell wall. ScPlc1, the only Plc1 in S. cerevisiae, like CnPlc1, lacks a secretory signal leader peptide.
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T Cell and Dendritic Cell Immune Responses to Cryptococcus
- Authors: Karen L. Wozniak, Stuart M. Levitz
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Source: Cryptococcus , pp 387-396
Publication Date :
January 2011
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Abstract:
This chapter reviews current knowledge regarding the role of dendritic cells (DCs) and T cells in the generation of protective immunity against Cryptococcus neoformans infections. DCs function as sentinels in the innate immune system. They are the most effective antigenpresenting cells (APCs) for inducing cell-mediated immune responses and are uniquely capable of activating naive T cells. DCs phagocytose pathogens, endocytose foreign antigens, process and present antigens to T cells, and are key mediators in the initiation of adaptive immune responses. DCs are uniquely capable of decoding fungal-associated information and translating it into different adaptive Th-type immune responses. The protective immune responses correlated with accumulation of myeloid DCs in the draining lymph nodes, while nonprotective responses were associated with accumulation of lymphoid DCs. Peripheral blood mononuclear cells from HIV-infected donors have profoundly impaired proliferative and cytokine responses to cryptococcal antigens. Immunization of mice with heat-killed C. neoformans conferred protection against challenge in wild-type mice but did not induce protection in nude mice (lacking T cells), demonstrating the importance of T cells in protection in the central nervous system (CNS). The lungs and brain are the most common sites of infection for C. neoformans and C. gattii. In pulmonary, systemic, and CNS infections, Th1-type cytokines are required for a protective cell-mediated immune response. The necessity of T cells for host defenses against cryptococcosis has prompted research into identifying immunoreactive cryptococcal antigens that could serve as vaccine candidates and as diagnostic reagents to measure T-cell responses in infected or at-risk patients.
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Acquired Immunity: Fungal Infections
- Author: Luigina Romani
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Source: The Immune Response to Infection , pp 289-299
Publication Date :
January 2011
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The most common of the human diseases caused by fungi are the opportunistic fungal infections that occur in patients with defective immunity. This chapter attempts to position the new findings on acquired immunity and fungi within the conceptual framework of a two-component antifungal response that includes resistance and tolerance. Resistance and tolerance are two types of host defense mechanisms that increase fitness in response to fungi. The enzyme indoleamine 2,3-dioxygenase (IDO) and tryptophan metabolites contribute to immune homeostasis by inducing Tregs and taming heightened inflammatory responses. The new entry, the Th17 pathway, playing an inflammatory role previously attributed to uncontrolled Th1 cell reactivity and Tregs and capable of fine-tuning protective antimicrobial immunity in order to minimize harmful immune pathology, have become an integral component of the immune response to fungi. In their capacity to induce Tregs and inhibit Th17, IDO and kynurenines pivotally contribute to cell lineage decision in experimental fungal infections and reveal an unexpected potential in the control of inflammation, allergy, and Th17-driven inflammation in these infections. Serological and skin reactivity surveys indicate the development of acquired cell-mediated immunity (CMI) to fungi. A number of clinical observations suggest an inverse relationship between interferon (IFN)-γ and interleukin (IL)-10 production in patients with fungal infections. The implication for IDO in immunoregulation in fungal infections has several important implications.
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Acquired Immunity to Intracellular Protozoa
- Authors: Phillip Scott, Eleanor M. Riley
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Source: The Immune Response to Infection , pp 301-311
Publication Date :
January 2011
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The control of pathogenic intracellular protozoa is dependent upon both an innate and acquired (or adaptive) immune response. Innate immune responses play an important role by controlling the early replication of parasites, giving time for acquired immunity to develop, although innate immune responses are rarely able to provide sufficient protection to prevent disease. Understanding how protective immunity can be induced, as well as knowing the mechanisms used by these intracellular parasites to avoid destruction, is critical for the development of new therapies as well as vaccines. This chapter investigates the acquired immune responses important in the control of four intracellular protozoans: Plasmodium, Leishmania, Toxoplasma gondii, and Trypanosoma cruzi. Acquired immunity to malaria is frequently described as being either antiparasite immunity, encompassing effector mechanisms that kill and clear parasites or parasite-infected cells, or clinical (or antitoxic) immunity. It is widely believed that acquired immunity to malaria rapidly wanes in the absence of frequent reinfection. A recent review suggests that previously immune individuals who become infected after spending long periods in nonendemic areas may develop mild-to-moderate symptoms of malaria despite having very low parasitemia.
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Immune Evasion by Parasites
- Authors: John M. Mansfield, Martin Olivier
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Source: The Immune Response to Infection , pp 453-469
Publication Date :
January 2011
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This chapter examines several mechanisms by which two well-known protozoan pathogens, one extracellular and one intracellular, successfully evade host immunity. It discusses how one protozoan parasite has evolutionarily addressed few problems by displaying a highly ordered molecular surface coat that serves largely to protect therypanosome plasma membrane from immunological assault. Many successful parasites exhibit antigenic variation to avoid immune elimination during infection. The most well-known example of immune evasion by parasites is antigenic variation by the African trypanosome, which for nearly a century has provided the classical paradigm for microbial antigenic variation as a means of escaping host immunity. In addition to an apparent absence of variant surface glycoprotein (VSG) C-terminal peptide processing by antigen-presenting cell (APCs) following primary exposure, there is evidence that the processing of parasite antigens may be more broadly regulated during progressive infection. Leishmania parasites infect host macrophage cells during their life cycle. Development of effective cell-mediated immune responses to these organisms requires that infected macrophages induce significant Th1 cell activation against leishmanial antigens. Parasitic protozoa regulate almost every aspect of host innate and adaptive immunity, and have evolved multiple mechanisms that permit passive and active evasion of host resistance. These mechanisms include not only the expression of variant antigens and specialized surface coats (African trypanosomes), but also the modulation of antigen expression and signaling pathways of the cells that they infect or interact with (trypanosomesand Leishmania spp.), effectively subverting or suppressing cellular mechanisms that can affect parasite survival.
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Trypanosomatidae: Leishmania Species, Trypanosoma cruzi (Chagas Disease), and Associated Complications
- Author: Jean-Pierre Dedet
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Source: Sequelae and Long-Term Consequences of Infectious Diseases , pp 275-289
Publication Date :
January 2009
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Abstract:
This chapter explains the postinfectious sequelae and long-term consequences of leishmaniasis and Chagas disease. A section discusses the long-term consequences and sequelae of leishmaniasis, with special emphasis on the long-term evolution of visceral leishmaniasis (VL) of immunosuppressed patients, post-kala-azar dermal leishmaniasis, the complications and scars resulting from localized CL (LCL), some particularly long-lasting forms of CL, and mucosal involvement of mucocutaneous leishmaniasis (MCL) and their disfiguring involvement and further sequelae. Treatment of all the leishmaniases remains difficult, due to the multiplicity of the existing Leishmania species and their variable susceptibility to the available drugs, which are old, toxic, and expensive products. Chagas disease is an infectious disease resulting from the parasitism of humans by Trypanosoma cruzi, a parasite of wild and domestic mammals, transmitted by blood-sucking triatomine bugs. The major causes of morbidity and mortality at the chronic stage are cardiac involvement, referred as chronic Chagas heart disease, and the “mega”-syndromes of the gastrointestinal tract. The major indications of the two specific trypanocidal drugs are in the acute phase of Chagas disease when diagnosed, congenital infection and prevention of accidental laboratory infections.
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Mumps Virus
- Author: John W. Gnann, Jr.
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Source: Clinical Virology, Third Edition , pp 877-888
Publication Date :
January 2009
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Abstract:
Mumps virus is classified as a member of the order Mononegavirales, family Paramyxoviridae, subfamily Paramyxovirinae, and genus Rubulavirus. Penetration of mumps virus virions into target cells begins with binding of the hemagglutininneuraminidase (HN) surface glycoprotein to sialic acid-containing receptors on the cell surface. Humans can be experimentally infected by inoculation of mumps virus onto the nasal or buccal mucosa, suggesting that natural infection results from airborne spread of droplets of respiratory secretions from infected to susceptible individuals. Mumps virus can establish persistent infection in neuronal cell lines and chronic central nervous system (CNS) infection in animal models, but it does not routinely cause chronic infections in humans. In the suckling hamster model, mumps virus CNS infection is associated with the development of stenosis of the sylvian aqueduct and with granular ependymitis. The majority of mumps patients with CNS involvement will have signs of meningeal irritation but no evidence of cortical dysfunction. The pathogenesis of mumps-related arthritis is uncertain; virus has not been isolated from joint fluid, and there is no evidence of immune complex deposition. Although clinical experience with this assay is currently limited, reverse transcriptase (RT)-PCR is likely to become the diagnostic method of choice for mumps virus CNS infection. Therapy of patients with uncomplicated mumps consists of conservative measures to provide symptomatic relief, such as analgesics, antipyretics, rest, and hydration. Symptomatic measures to alleviate the pain and swelling of mumps orchitis include bed rest, scrotal support and opioid analgesics.
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Rubella Virus
- Author: David W. Kimberlin
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Source: Clinical Virology, Third Edition , pp 1275-1289
Publication Date :
January 2009
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Rubella virus is the sole member of the Rubivirus genus of the Togaviridae family. The other genus in the family of Togaviridae is Alphavirus. In contrast to the alphaviruses, which replicate in arthropods and in vertebrates, rubella virus has no invertebrate hosts. As humans are the only known natural host for rubella virus, the virus must circulate continuously within populations of people between periods of epidemics. While direct cellular destruction by rubella virus accounts for some of the tissue damage seen in congenital rubella syndrome, vascular injury and resulting insufficiency are more important in the pathogenesis of congenital defects. The consequences of in utero rubella virus infection can be considered broadly as belonging to one of three categories: (i) signs and symptoms that are transiently apparent in affected infants, (ii) permanent manifestations that are noted within the first year of life, and (iii) manifestations of congenital rubella that are delayed in onset until later in life (2 years of age to adulthood). Rubella virus infection is definitively diagnosed by isolation of rubella virus in tissue culture, using one of several cell lines and primary cell strains. Viral interference in African green monkey kidney (AGMK) cells is one common culture technique by which the presence of rubella virus is demonstrated.
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Cytokines and Macrophages and Dendritic Cells: Key Modulators of Immune Responses
- Authors: Frank Kaiser, Anne O’Garra
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Source: Phagocyte-Pathogen Interactions , pp 281-299
Publication Date :
January 2009
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This chapter discusses the fundamental role of phagocytes, with specific emphasis on macrophages and dendritic cells (DCs), as potent cytokine producers and responders, establishing them as primary effector cells as well as regulators of innate and adaptive immune responses. It draws attention to the role of T-cell-derived cytokines produced during adaptive Th1 and Th2 responses, IFN-γ and IL-4/IL-13, respectively, and their fundamental role in modulating macrophage and DC function. The chapter also discusses the cellular and molecular mechanisms that enable macrophages and DCs to express complex cytokine patterns in response to pathogens, which are key to mounting effective innate and downstream adaptive immune responses. The cellular response induced by the engagement of PRRs is often referred to as the “innate” activation of phagocytes, in contrast to the “classical” and “alternative” activation of macrophages by cytokines. IL-4 and IL-13 also induce intracellular enzymes that are implicated in cell recruitment and granuloma formation. Therefore, the distinctive macrophage phenotype induced by the Th2-type cytokines IL-4 and IL-13, also referred to as alternatively activated macrophages, plays an important role in dampening classical cell-mediated immune responses while reprogramming the response toward an appropriate type that promotes an efficient eradication of extracellular pathogens. Recognition of microorganisms or their products initiates complex signaling pathways in these cells that determine the pattern of cytokines produced and the subsequent effector response, critical for the eradication of pathogens with minimum damage to the host.
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Of Mice and Men
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Source: The Elusive Malaria Vaccine , pp 234-283
Publication Date :
January 2009
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Abstract:
Human malaria does not lend itself easily to basic research in immunology, so a convenient laboratory model for in vivo studies of mammalian malaria was desirable. The need was satisfied with the description of a rodent malaria parasite, P. berghei, by a Belgian physician (Ignace Vincke) and entomologist. One of Jerome Vanderberg's most valuable findings was his observation that upon in vitro exposure to serum from immunized mice, an antibody-mediated precipitation occurred around sporozoites and the precipitate projected from one end. The injection of irradiated sporozoites by mosquitoes should thus be viewed as an attempt to test the feasibility of vaccination in humans, which if successful could lead to trials using more practical techniques. The results showed that mice so immunized were completely protected from sporozoite challenges that caused blood infections and death in 100% of nonimmunized control mice. Using the mouse malaria model, P. yoelii, it was shown that after mosquito inoculation the irradiated sporozoites are deposited in the skin and then move into the regional lymph nodes, where, after dendritic cell presentation, T cells were primed to recognize the parasite.
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16 The Constituents of the Cell Envelope and Their Impact on the Host Immune System
- Authors: Warwick J. Britton, James A. Triccas
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Source: The Mycobacterial Cell Envelope , pp 249-270
Publication Date :
January 2008
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Abstract:
This chapter focuses on recent developments in one’s understanding of how different components of the cell envelope from virulent mycobacteria, in particular Mycobacterium tuberculosis, interact with each stage of innate and adaptive immune responses. Human dendritic cells express an additional C-type lectin, dendritic cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN), which is not present on macrophages but serves as a major receptor for M. tuberculosis on dendritic cells (DCs). Cell wall components of mycobacteria bind to these pathogen recognition receptors on DCs and macrophages, and initiate the host response to infection. The biological relevance of TLR activation by cell wall components has been examined by mycobacterial infection of gene-deficient mice. Inactivation of protein kinase G (PknG) by gene disruption or chemical inhibition resulted in delivery of pathogenic mycobacteria to lysosomes and mycobacterial killing, and conversely, expression of PknG in nonpathogenic prevented phagosomal maturation. The induction of adaptive immunity to mycobacteria and activation of infected macrophages by IFN-γ can overcome the maturation arrest of mycobacteria containing phagosomes. CD1 proteins, which are antigen presenting molecules encoded by genes located outside of the major histocompatibility complex (MHC), recognize nonpeptide lipid or glycolipid structures, including components of mycobacteria. The containment of mycobacterial infection requires the formation of granulomas (or tubercles), which are nodular aggregations of lymphocytes, macrophages, and epithelioid cells. In human M. tuberculosis infection, the propensity of trehalose dimycolate (TDM) and other cell wall components to promote granuloma formation in association with a chronic T-cell response leads to caseating granulomas, which may erode into airways.
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Overall Features of HIV Pathogenesis: Prognosis for Long-Term Survival
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Source: HIV and the Pathogenesis of AIDS, Third Edition , pp 317-361
Publication Date :
January 2007
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HIV pathogenesis reflects the various biologic properties of HIV and the host’s immune response to the virus. The differential expression of these two major components of HIV infection determines the final outcome: long-term survival or development of AIDS with its associated opportunistic infections and cancers. How these viral and immunological features of HIV pathogenesis influence survival from HIV infection becomes an important consideration. This chapter first discusses cofactors in HIV infection and disease progression. The pathogenic pathway, after the acute infection period, can be divided into three major phases: early period following acute virus infection, persistent period, and symptomatic period. One noteworthy observation is the loss of CD4+ T cells in the bowel of SIV-infected healthy sooty mangabeys similar to that noted in HIV infection. The chapter talks about high-risk HIV-exposed seronegative individuals, and diversity of viruses involved in transmission and infection. In addition to the studies on R5 versus X4 pathogenesis, several experiments have been initiated to determine if some HIV-1 subtypes distinguished by specific biologic and serologic features are associated with pathology in certain tissues. Three major tissues with potential virus subtypes are reviewed, but others could eventually include HIV-1 isolates isolated from the heart, lung, kidney, and endocrine organs.
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Leishmaniasis
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Source: Diagnostic Medical Parasitology, Fifth Edition , pp 190-217
Publication Date :
January 2007
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Abstract:
Leishmaniasis refers to a diverse group of diseases, with the spectrum of disease depending on the infecting species. Leishmania major, L. tropica, L. aethiopica, and, rarely, L. infantum cause cutaneous disease in the Old World; disease manifestations include nodular and ulcerative skin lesions. Lesions usually occur on exposed parts of the body such as the face, hands, feet, arms, and legs; uncommon sites include the ears, tongue, and eyelids. Lymphatic spread may occur in L. major infections, with subcutaneous nodules in a linear distribution and regional lymphadenopathy; if the initial lesion is on the hand, this clinical presentation may resemble sporotrichosis. The majority of AIDS patients present with the classical picture of visceral leishmaniasis (VL), but asymptomatic cutaneous leishmaniasis (CL), mucocutaneous leishmaniasis, “disseminated” CL (DCL), and post-kala-azar dermal leishmaniasis can be seen. The RK39 strip test is ideal for rapid reliable field diagnosis of VL. The test has high sensitivity and specificity; however, it remains positive long after treatment. L. chagasi causes subclinical infections and American visceral leishmaniasis (AVL), which is potentially fatal if not treated, and it has recently been associated with atypical cutaneous leishmaniasis (ACL) in Central America, particularly in Honduras. PCR will probably become the test of choice, as with other types of leishmaniasis, but the practicality and cost issues mean that routine methods will continue to be the most likely approach, particularly since the majority of cases are seen in more remote rural areas.
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