The p2x7 Purinergic Receptor and Mycobacterial Infections in Humans: The role of loss-of-function polymorphisms in the gene for the p2X7 purinergic receptor and mycobacterial infections in humans

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9783639012262: The p2x7 Purinergic Receptor and Mycobacterial Infections in Humans: The role of loss-of-function polymorphisms in the gene for the p2X7 purinergic receptor and mycobacterial infections in humans

Tuberculosis (TB) remains an enormous global health problem. The majority of people infected with Mycobacterium tuberculosis are able to contain their infection, however, in approximately 10% of individuals, active disease eventually develops, usually from reactivation of latent infection. HIV coinfection and other environmental causes of reduced T cell immunity predispose to this progression in a proportion of individuals.There is emerging evidence that genetic variation also influences susceptibility to TB. Activation of the P2X7 receptor kills mycobacteria within macrophages. Several polymorphisms in the P2X7 gene impair this killing. The most common of these polymorphisms was strongly associated with extrapulmonary TB in two separate cohorts in a Sydney population. Furthermore, ATP-mediated killing of mycobacteria was significantly impaired in macrophages from heterozygous subjects and ablated in macrophages from subjects homozygous for this polymorphism. By contrast, no loss-of-function polymorphism was associated with clinical leprosy in a Nepali population. P2X7-mediated killing of mycobacteria can be augmented with stimulation of certain cytokines.

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Suran Fernando is a Clinical Immunologist at Royal North Shore Hospital in Sydney, Australia. He obtained his Medical Degree in 1994 and then attained fellowships of the Royal Australasian Colleges of Physicians and Pathologists in 2001. As an NH&MRC scholar, he completed his doctoral thesis in the Mycobacterial Laboratory, Centenary Institute, Sydney in 2006

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Book Description Book Condition: New. Publisher/Verlag: VDM Verlag Dr. Müller | The role of loss-of-function polymorphisms in the gene for the p2X7 purinergic receptor and mycobacterial infections inhumans | Tuberculosis (TB) remains an enormous global health problem. The majority of people infected with Mycobacterium tuberculosis areable to contain their infection, however, in approximately 10% of individuals, active disease eventually develops, usually from reactivation of latent infection. HIV coinfection and other environmental causes of reduced T cell immunity predispose to this progression in a proportion of individuals. There is emerging evidence that genetic variation also influences susceptibility to TB. Activation of the P2X7 receptor kills mycobacteria within macrophages. Several polymorphisms in the P2X7 gene impair this killing. The most common of these polymorphisms was strongly associated with extrapulmonary TB in two separate cohorts in a Sydney population. Furthermore, ATP-mediated killing of mycobacteria was significantly impaired in macrophages from heterozygous subjects and ablated in macrophages from subjects homozygous for this polymorphism. By contrast, no loss-of-function polymorphism was associated with clinical leprosy in a Nepalipopulation. P2X7-mediated killing of mycobacteria can be augmented with stimulation of certain cytokines. | Format: Paperback | Language/Sprache: english | 375 gr | 272 pp. Bookseller Inventory # K9783639012262

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Book Description VDM Verlag Mai 2008, 2008. Taschenbuch. Book Condition: Neu. Neuware - Tuberculosis (TB) remains an enormous global health problem. The majority of people infected with Mycobacterium tuberculosis areable to contain their infection, however, in approximately 10% of individuals, active disease eventually develops, usually from reactivation of latent infection. HIV coinfection and other environmental causes of reduced T cell immunity predispose to this progression in a proportion of individuals. There is emerging evidence that genetic variation also influences susceptibility to TB. Activation of the P2X7 receptor kills mycobacteria within macrophages. Several polymorphisms in the P2X7 gene impair this killing. The most common of these polymorphisms was strongly associated with extrapulmonary TB in two separate cohorts in a Sydney population. Furthermore, ATP-mediated killing of mycobacteria was significantly impaired in macrophages from heterozygous subjects and ablated in macrophages from subjects homozygous for this polymorphism. By contrast, no loss-of-function polymorphism was associated with clinical leprosy in a Nepalipopulation. P2X7-mediated killing of mycobacteria can be augmented with stimulation of certain cytokines. 272 pp. Englisch. Bookseller Inventory # 9783639012262

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Book Description VDM Verlag Mai 2008, 2008. Taschenbuch. Book Condition: Neu. Neuware - Tuberculosis (TB) remains an enormous global health problem. The majority of people infected with Mycobacterium tuberculosis areable to contain their infection, however, in approximately 10% of individuals, active disease eventually develops, usually from reactivation of latent infection. HIV coinfection and other environmental causes of reduced T cell immunity predispose to this progression in a proportion of individuals. There is emerging evidence that genetic variation also influences susceptibility to TB. Activation of the P2X7 receptor kills mycobacteria within macrophages. Several polymorphisms in the P2X7 gene impair this killing. The most common of these polymorphisms was strongly associated with extrapulmonary TB in two separate cohorts in a Sydney population. Furthermore, ATP-mediated killing of mycobacteria was significantly impaired in macrophages from heterozygous subjects and ablated in macrophages from subjects homozygous for this polymorphism. By contrast, no loss-of-function polymorphism was associated with clinical leprosy in a Nepalipopulation. P2X7-mediated killing of mycobacteria can be augmented with stimulation of certain cytokines. 272 pp. Englisch. Bookseller Inventory # 9783639012262

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Book Description VDM Verlag Dr. Mueller e.K., Germany, 2008. Paperback. Book Condition: New. Language: English . Brand New Book ***** Print on Demand *****.Tuberculosis (TB) remains an enormous global health problem. The majority of people infected with Mycobacterium tuberculosis are able to contain their infection, however, in approximately 10 of individuals, active disease eventually develops, usually from reactivation of latent infection. HIV coinfection and other environmental causes of reduced T cell immunity predispose to this progression in a proportion of individuals. There is emerging evidence that genetic variation also influences susceptibility to TB. Activation of the P2X7 receptor kills mycobacteria within macrophages. Several polymorphisms in the P2X7 gene impair this killing. The most common of these polymorphisms was strongly associated with extrapulmonary TB in two separate cohorts in a Sydney population. Furthermore, ATP-mediated killing of mycobacteria was significantly impaired in macrophages from heterozygous subjects and ablated in macrophages from subjects homozygous for this polymorphism. By contrast, no loss-of-function polymorphism was associated with clinical leprosy in a Nepali population. P2X7-mediated killing of mycobacteria can be augmented with stimulation of certain cytokines. Bookseller Inventory # AAV9783639012262

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Book Description VDM Verlag Mai 2008, 2008. Taschenbuch. Book Condition: Neu. This item is printed on demand - Print on Demand Neuware - Tuberculosis (TB) remains an enormous global health problem. The majority of people infected with Mycobacterium tuberculosis areable to contain their infection, however, in approximately 10% of individuals, active disease eventually develops, usually from reactivation of latent infection. HIV coinfection and other environmental causes of reduced T cell immunity predispose to this progression in a proportion of individuals. There is emerging evidence that genetic variation also influences susceptibility to TB. Activation of the P2X7 receptor kills mycobacteria within macrophages. Several polymorphisms in the P2X7 gene impair this killing. The most common of these polymorphisms was strongly associated with extrapulmonary TB in two separate cohorts in a Sydney population. Furthermore, ATP-mediated killing of mycobacteria was significantly impaired in macrophages from heterozygous subjects and ablated in macrophages from subjects homozygous for this polymorphism. By contrast, no loss-of-function polymorphism was associated with clinical leprosy in a Nepalipopulation. P2X7-mediated killing of mycobacteria can be augmented with stimulation of certain cytokines. 272 pp. Englisch. Bookseller Inventory # 9783639012262

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Book Description VDM Verlag. Paperback. Book Condition: New. Paperback. 272 pages. Dimensions: 8.7in. x 5.9in. x 0.6in.Tuberculosis (TB) remains an enormous global health problem. The majority of people infected with Mycobacterium tuberculosis are able to contain their infection, however, in approximately 10 of individuals, active disease eventually develops, usually from reactivation of latent infection. HIV coinfection and other environmental causes of reduced T cell immunity predispose to this progression in a proportion of individuals. There is emerging evidence that genetic variation also influences susceptibility to TB. Activation of the P2X7 receptor kills mycobacteria within macrophages. Several polymorphisms in the P2X7 gene impair this killing. The most common of these polymorphisms was strongly associated with extrapulmonary TB in two separate cohorts in a Sydney population. Furthermore, ATP-mediated killing of mycobacteria was significantly impaired in macrophages from heterozygous subjects and ablated in macrophages from subjects homozygous for this polymorphism. By contrast, no loss-of-function polymorphism was associated with clinical leprosy in a Nepali population. P2X7-mediated killing of mycobacteria can be augmented with stimulation of certain cytokines. This item ships from multiple locations. Your book may arrive from Roseburg,OR, La Vergne,TN. Paperback. Bookseller Inventory # 9783639012262

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