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Gotowe bibliografie tematyczne / Cell Mediated Immunity (CMI) / Książki

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Książki na temat „Cell Mediated Immunity (CMI)”

Autor: Grafiati

Data publikacji: 3 czerwca 2025

Data aktualizacji: 31 lipca 2025

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Sprawdź 24 najlepszych książek naukowych na temat „Cell Mediated Immunity (CMI)”.

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1

Takeshi, Yoshida, ed. Investigation of cell-mediated immunity. Churchill Livingstone, 1985.

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2

L, Goddeeris Bruno M., and Morrison W. Ivan, eds. Cell-mediated immunity in ruminants. CRC Press, 1994.

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3

1943-, Watson James D., and Marbrook John, eds. Recognition and regulation in cell-mediated immunity. M. Dekker, 1985.

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4

H, Fridman Wolf, and Sautés Catherine, eds. Cell-mediated effects of immunoglobulins. Springer, 1997.

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5

Huttunen, Kaisa. Cell-mediated immunity in renal patients: An in vitro study. University of Oulu, 1985.

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6

Toft, Palle. The effect of surgical stress, endotoxin induced sepsis and extracorporeal circulation on the cell mediated immunity. Faculty of Health Sciences, University of Aarhus, 2002.

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7

1936-, Lotzová Eva, and Herberman Ronald B. 1940-, eds. Immunobiology of natural killer cells. CRC Press, 1986.

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8

1940-, Herberman Ronald B., Callewaert Denis M, and International Workshop on NK Cells (3rd : 1984 : Oakland University), eds. Mechanisms of cytotoxicity by NK cells. Academic Press, 1985.

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9

Herberman, Ronald. Natural Cell-Mediated Immunity Against Tumors. Elsevier Science & Technology Books, 2012.

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10

Bloom, Barry R., and Philip R. Glade. In Vitro Methods in Cell-Mediated Immunity. Elsevier Science & Technology Books, 2014.

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11

Fridman, Wolf H. Cell-Mediated Effects of Immunoglobulins. Springer London, Limited, 2012.

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12

London, University of, ed. The role of cell-mediated immunity in protection against infectious Bursal disease virus. 1997.

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13

Carabin Is a Negative Regulator of Cd8+ T-cell-mediated Anti-tumor Immunity. [publisher not identified], 2022.

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14

Lotzova, Eva, and Ronald B. Herberman. Immunobiology of Natural Killer Cells: Volume 2. Taylor & Francis Group, 2019.

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15

Lotzova, Eva, and Ronald B. Herberman. Immunobiology of Natural Killer Cells: Volume 2. Taylor & Francis Group, 2019.

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16

Lotzova, Eva, and Ronald B. Herberman. Immunobiology of Natural Killer Cells: Volume 2. Taylor & Francis Group, 2019.

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17

Lotzova, Eva, and Ronald B. Herberman. Immunobiology of Natural Killer Cells: Volume 2. Taylor & Francis Group, 2019.

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18

Lotzova, Eva, and Ronald B. Herberman. Immunobiology of Natural Killer Cells: Volume 2. Taylor & Francis Group, 2019.

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19

PODACK, E. ED. Cytotoxic Effector Mechanisms (Current Topics in Microbiology & Immunology). Springer, 1989.

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20

Eljaafari, Assia, and Pierre Miossec. Cellular side of acquired immunity (T cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0049.

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The adaptive T-cell response represents the most sophisticated component of the immune response. Foreign invaders are recognized first by cells of the innate immune system. This leads to a rapid and non-specific inflammatory response, followed by induction of the adaptive and specific immune response. Different adaptive responses can be promoted, depending on the predominant effector cells that are involved, which themselves depend on the microbial/antigen stimuli. As examples, Th1 cells contribute to cell-mediated immunity against intracellular pathogens, Th2 cells protect against parasites,

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21

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0074_update_001.

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Individuals appear to be predisposed to antiglomerular basement membrane (anti-GBM) disease by carrying a predisposing human leucocyte antigen type, DRB1*1501 being identified as the highest risk factor, and there are likely to be other predisposing genes or influences on top of which a relatively rare ‘second hit’ leads to the development of autoimmunity. In anti-GBM disease this appears to have a self-perpetuating, accelerating component, that may be to do with antibodies and altered antigen presentation. Lymphocyte depletion may also predispose to the disease. A number of second hits have b

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22

Dambuza, Ivy M., Jeanette Wagener, Gordon D. Brown, and Neil A. R. Gow. Immunology of fungal disease. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0009.

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Advances in modern medicine, such as organ transplantations and the appearance of HIV (human immunodeficiency virus), have significantly increased the patient cohort at risk of developing chronic superficial and life-threatening invasive fungal infections. To tackle this major healthcare problem, there is an urgent need to understand immunity against fungal infections for the purposes of vaccine design or immune-mediated interventions. In this chapter, we give an overview of the components of the innate and adaptive immune system and how they contribute to host defence against fungi. The vario

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23

Gilden, Don, Randall J. Cohrs, Ravi Mahalingam, and Maria A. Nagel. Varicella Zoster Virus Infection of the Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0149.

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Varicella zoster virus (VZV) is a human herpesvirus that causes varicella (chickenpox), after which virus becomes latent in ganglionic neurons along the entire neuraxis. Reactivation of VZV due to a decline in the cell-mediated immune response to VZV in elderly or immunocompromised individuals causes zoster (shingles), frequently complicated by chronic pain (postherpetic neuralgia) and serious neurological disease (meningoencephalitis, myelitis and VZV vasculopathy due to retrograde spread of virus after zoster. Here, we describe clinical, laboratory and pathological features of neurological c

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24

Izzedine, Hassan, and Victor Gueutin. Drug-induced acute tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0084.

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Drug-induced acute tubulointerstitial nephritis (ATIN) is the most common aetiology of ATIN and a potentially correctable cause of acute kidney injury (AKI). An interval of 7–10 days typically exists between drug exposure and development of AKI, but this interval can be considerably shorter following re-challenge or markedly longer with certain drugs. It occurs in an idiosyncratic and non-dose-dependent manner. Antibiotics, NSAIDs, and proton pump inhibitors are the most frequently involved agents, but the list of drugs that can induce ATIN is continuously increasing. The mechanism of renal in

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