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Książki na temat „Macrophage activation”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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1

Russell, Stephen W., and Siamon Gordon, eds. Macrophage Biology and Activation. Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77377-8.

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2

W, Russell Stephen, and Gordon Siamon, eds. Macrophage biology and activation. Springer-Verlag, 1992.

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3

1955-, Suttles Jill, ed. T-cell signaling of macrophage activation: Cell contact-dependent and cytokine signals. R.G. Landes, 1995.

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4

Pulkki, Kari. Activation of synovial fibroblasts by macrophage-derived factors: Characterization of arthritis-associated and cytokine-induced biochemical and morphological changes in cultured synovial fibroblasts. K. Pulkki, 1988.

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Kucey, Daryl Stanton. Modulation of macrophage procoagulant activity by platelet activating factor. National Library of Canada = Bibliothèque nationale du Canada, 1992.

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6

Adams, Dolph O. Macrophage Activation. Springer, 2013.

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7

Adams, Dolph O. Macrophage Activation. Springer, 2013.

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8

Grom, Alexei A., and Athimalaipet V. Ramanan. Macrophage activation syndrome. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0168.

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Macrophage activation syndrome (MAS) is a life-threatening condition caused by excessive activation and proliferation of T lymphocytes and haemophagocytic macrophages. Although MAS has been reported in association with almost any rheumatic disease, it is by far most common in systemic juvenile idiopathic arthritis. Flares of the underlying disease or infection are most common triggers of MAS. The pathognomonic feature of MAS is typically found in bone marrow: numerous, well-differentiated macrophagic histiocytes phagocytosing normal haematopoietic elements. The expansion of these histiocytes l

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9

The human macrophage system: Activity and functional morphology. Karger, 1988.

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10

Gordon, Siamon, and Stephen W. Russell. Macrophage Biology and Activation. Springer London, Limited, 2011.

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11

Gordon, Siamon, and Stephen W. Russell. Macrophage Biology and Activation. Springer London, Limited, 2012.

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12

Macrophage Biology and Activation. Island Press, 1992.

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13

Hussain Bhat, Khalid, ed. Macrophage Activation - Biology and Disease. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.79065.

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14

Russell, Stephen W. Macrophage Biology and Activation (Current Topics in Microbiology and Immunology). Springer, 1992.

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15

Bucala, Richard. Mif Handbook. World Scientific Publishing Co Pte Ltd, 2012.

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16

Bucala, Richard. Mif Handbook. World Scientific Publishing Co Pte Ltd, 2012.

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17

Stout, Robert D. T-Cell Signaling of Macrophage Activation: Cell Contact-Dependent and Cytokine Signals (Archives of Toxicology). Springer, 1996.

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18

Russell, S., and S. Gordon. Current Topics in Microbiology and Immunology: Macrophage Biology and Activation (Current Topics in Microbiology and Immunology). Springer-Verlag Berlin and Heidelberg GmbH & Co. KG, 1992.

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19

Tsai, Ching-Wei, Sanjeev Noel, and Hamid Rabb. Pathophysiology of Acute Kidney Injury, Repair, and Regeneration. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0030.

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Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of

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20

Pitzalis, Costantino, Frances Humby, and Michael P. Seed. Synovial pathology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0052.

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Synovial pathology is seen in a variety of disease states, including rheumatoid arthritis (RA), osteoarthritis (OA), psoriatic arthritis, and systemic lupus erythmatosus (SLE). This chapter highlights recent advances that characterize the cellular composition of these tissues according to surface markers and chemokine and cytokine expression, and describes synovial functional status and response to therapeutics. In RA, after initiation, pannus migrates over and under cartilage, and into subchondral bone, in a destructive process. Cartilage-pannus junction (CPJ) is characterized as invasive or

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21

Murphy, Claire Louise, Yiannis Ioannou, and Nicola Ambrose. Juvenile systemic lupus erythematosus. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198739180.003.0008.

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Juvenile-onset systemic lupus erythematosus (JSLE) is similar to adult-onset SLE, but there are distinct differences in clinical features, serology, and management requirements. It is more aggressive than adult-onset SLE with frequent renal and haematological manifestations and higher mortality rates. The cause of JSLE is unknown but appears to be multifactorial with genetic, immunological, hormonal, and environmental influences. Macrophage activation syndrome is a potentially life-threatening complication, and may mimic the underlying disease or be confused with sepsis. Transferring care from

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22

Badimon, Lina, Felix C. Tanner, Giovanni G. Camici, and Gemma Vilahur. Pathophysiology of thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0018.

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Ischaemic heart disease and stroke are major causes of death and morbidity worldwide. Coronary and cerebrovascular events are mainly a consequence of a sudden thrombotic occlusion of the vessel lumen. Arterial thrombosis usually develops on top of a disrupted atherosclerotic plaque because of the exposure of thrombogenic material, such as collagen fibrils and tissue factor (TF), to the flowing blood. TF, either expressed by subendothelial cells, macrophage- and/or vascular smooth muscle-derived foam-cells in atherosclerotic plaques, is a key element in the initiation of thrombosis due to its a

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23

Sebastio, Gianfranco, Manuel Schiff, and Hélène Ogier de Baulny. Lysinuric Protein Intolerance and Hartnup Disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0025.

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Lysinuric protein intolerance (LPI) is an inherited aminoaciduria caused by defective cationic amino acid transport at the basolateral membrane of epithelial cells in intestine and kidney. LPI is caused by mutations in the SLC7A7 gene, which encodes the y+LAT-1 protein, the catalytic light chain subunit of a complex belonging to the heterodimeric amino acid transporter family. Symptoms usually begin after weaning with refusal of feeding, vomiting, and consequent failure to thrive. Hepatosplenomegaly, hematological anomalies, and neurological involvement including hyperammonemic coma will progr

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24

Baildam, Eileen. Juvenile idiopathic arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0116.

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Juvenile idiopathic arthritis (JIA) is defined as arthritis lasting for 6 weeks or more presenting in childhood at any age up to 17 years. Arthritis is diagnosed clinically by the presence of joint pain, stiffness, and swelling with inflammation limiting the range of individual joint movement. There are subtypes that tend to follow distinct courses and with phenotypes that vary widely from a serious systemic inflammatory disorder of systemic JIA to single-joint monoarthritis. The differential diagnosis of JIA is wide and the best chance of long-term remission is where treatment is started as e

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25

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across

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26

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and

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27

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and

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28

Landmesser, Ulf, and Wolfgang Koenig. From risk factors to plaque development and plaque destabilization. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0003.

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This chapter begins with a discussion of recent vascular research that has unveiled the complex interaction between exposure to risk factors and pathological changes at the vessel wall. Risk factors such as smoking or hyperlipidaemia first cause a pre-morbid phenotype with reversible dysfunction of flow-mediated vasodilation, known as endothelial dysfunction (ED). If exposure to risk factor(s) does not cease, ED develops into the first morphological vascular changes that finally lead to atherosclerosis. Cholesterol crystals have been shown to lead to pro-inflammatory activation of macrophages.

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29

Michaels, Frank H. Studies of the effects of infection by caprine arthritis-encephalitis virus of synovial macrophages: Activation, loss of accessory cell capability and increased expression of virus. 1989.

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30

Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.

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Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling

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