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Books on the topic 'Mucosal immune system'

Author: Grafiati
Published: 4 June 2021
Last updated: 26 January 2023

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1

Å, Hanson Lars, and Svanborg-Edén Catharina, eds. Mucosal immunobiology: Cellular-molecular interactions in the mucosal immune system. Basel: Karger, 1988.

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2

Mucosal immunity. San Diego, CA: Academic Press, 2010.

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3

Dayan, Nava, and Philip W. Wertz, eds. Innate Immune System of Skin and Oral Mucosa. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118025338.

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4

1951-, MacDonald Thomas T., ed. Ontogeny of the immune system of the gut. Boca Raton, Fla: CRC Press, 1990.

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5

Falk Symposium (133rd 2004 Berlin, Germany). Mechanisms of intestinal inflammation: Implications for therapeutic intervention in IBD : proceedings of Falk Symposium 133 (New Findings on Pathogenesis and Progress in Management of Inflammatory Bowel Diseases, Part I) held in Berlin, Germany, June 10-11, 2003. Dordrecht: Kluwer Academic Publishers, 2004.

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6

Derek, Chadwick, and Goode Jamie, eds. Inflammatory bowel disease: Crossroads of microbes, epithelium, and immune systems. Chichester, UK: J. Wiley, 2004.

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7

Innate immune system of skin and oral mucosa: Properties and impact in pharmaceutics, cosmetics, and personal care products. Hoboken, N.J: John Wiley & Sons, 2011.

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8

Hanson, Lars A. Nobel Symposium No 68, Mucosal Immunobiology: Cellular-Molecular Interactions in the Mucosal Immune System (Monographs in Allergy). S Karger Pub, 1988.

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9

Bourne, F. J. Mucosal Immune System: Proceedings of a Seminar in the EEC Programme of Coordination of Agricultural Research on Protection of the Young Animal Against Perinatal Diseases, Held at the University of Bristol, School of Veterinary Science, Langford, Nr. Bristol, United Kingdom on September 9-11 1980. Springer, 2012.

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10

Bourne, F. J. Mucosal Immune System: Proceedings of a Seminar in the Eec Programme of Coordination of Agricultural Research on Protection of the Young Animal Against Perinatal Diseases, Held at the University of Bristol, School of Veterinary Science, Langford, Nr. Bristol, United Kingdom on September 9–11 1980. Springer, 2011.

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11

(Editor), Richard Blumberg, and Markus F. Neurath (Editor), eds. Immune Mechanisms in Inflammatory Bowel Disease (Advances in Experimental Medicine and Biology). Springer, 2006.

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12

Dayan, Nava, and Philip W. Wertz. Innate Immune System of Skin and Oral Mucosa. Wiley & Sons, Incorporated, John, 2011.

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13

Frenkel, Joost, and Hans R. Waterham. Mevalonate Kinase Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0039.

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Mevalonate kinase deficiency (MKD) is an autosomal recessive inborn error of isoprenoid biosynthesis, a pathway yielding sterols and nonsterol isoprenoids.In patients, the enzyme activity of mevalonate kinase is severely reduced due to mutations in the encoding gene, MVK. The substrate, mevalonate, accumulates and is elevated in blood and urine. Shortage of certain downstream products of the pathway, nonsterol isoprenoids, leads to dysregulation of the innate immune system, activation of inflammasomes, and interleukin (IL)-1 mediated inflammation.Symptoms start in early childhood with recurrent attacks of fever, vomiting, diarrhea, headache, sore throat, abdominal pain, arthralgias, painful lymphadenopathy, hepatosplenomegaly, skin rash, and mucosal ulcers. Severely affected patients have additional symptoms, such as intellectual impairment, progressive cerebellar ataxia, and tapetoretinal degeneration. Complications include intestinal obstruction, AA-amyloidosis, hemophagocytosis, and severe infection.Management of MKD is directed at controlling inflammation.
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14

Blaser, Annika Reintam, and Adam M. Deane. Normal physiology of the gastrointestinal system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0172.

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The gastrointestinal (GI) system is responsible for digestion and absorption, but also has important endocrine, immune and barrier functions. Additionally, the GI system plays a major role in fluid, electrolyte and acid-base balance. The GI system is regulated by complex myogenic, neural and humoral mechanisms, and, in health, these are affected by the presence of luminal nutrient, thereby modulating function of the GI system. Accordingly, GI function varies depending on whether a person is fasted or in the postprandial state. Adequate fasting and postprandial perfusion, motility and exocrine secretion are required for ‘normal’ functioning. The protective mechanisms of the GI system consist of physical (intact gut mucosa), non-immune (gastric acid, intestinal mucin, bile and peristalsis) and immune (gut-associated lymphoid tissue, GALT) elements. Disruption of GI protection is a putative mechanism underlying the development of multiple-organ dysfunction syndrome. Maintenance of GI function is increasingly recognised as an important factor underlying survival in critical illness.
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15

Foundation, Novartis. Inflammatory Bowel Disease: Crossroads of Microbes, Epithelium and Immune Systems (Novartis Foundation Symposia). Wiley, 2005.

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16

Dayan, Nava, and Philip W. Wertz. Innate Immune System of Skin and Oral Mucosa: Properties and Impact in Pharmaceutics, Cosmetics, and Personal Care Products. Wiley & Sons, Incorporated, John, 2012.

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17

Dayan, Nava, and Philip W. Wertz. Innate Immune System of Skin and Oral Mucosa: Properties and Impact in Pharmaceutics, Cosmetics, and Personal Care Products. Wiley & Sons, Incorporated, John, 2011.

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18

Dayan, Nava, and Philip W. Wertz. Innate Immune System of Skin and Oral Mucosa: Properties and Impact in Pharmaceutics, Cosmetics, and Personal Care Products. Wiley & Sons, Incorporated, John, 2011.

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19

Bowman, Simon, John Hamburger, Elizabeth Price, and Saaeha Rauz. Sjögren’s syndrome—clinical features. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0127.

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Sjögren's syndrome is a chronic, immune-mediated, condition of unknown aetiology characterized by focal lymphocytic infiltration of exocrine glands associated with dry mouth and eyes. It occurs in its own right (primary Sjögren's syndrome, pSS), or as a late feature of other rheumatic diseases such as rheumatoid arthritis, systemic lupus erythematosus or scleroderma (secondary Sjögren's syndrome). There is a strong female bias. pSS typically affects women in their middle years with an estimated prevalence of 0.1–0.6%. 75% of patients have anti-Ro and/or anti-La antibodies, often with raised immunoglobulin levels (hypergammaglobulinaemia). In patients without these antibodies the diagnosis can be confirmed by salivary gland biopsy. Treatment is generally symptomatic using artificial tears, saliva replacements/stimulants and good dental hygiene. Three-quarters of patients with pSS report significant fatigue with a negative impact on quality of life. This can be the most disabling symptom. Approximately 20% of patients develop systemic features including persistent salivary gland swelling, cutaneous vasculitis, peripheral neuropathy, interstitial lung disease, autoimmune cytopenias or renal tubular acidosis. Hydroxychloroquine and corticosteroids are the most widely used therapies for systemic features. There is a 44fold increased risk of mucosa-associated lymphoid tissue (MALT) B-cell lymphoma in pSS, typically affecting the salivary glands. On account of abnormalities in the B-cell system in pSS there is current interest in the use of anti-B-cell directed monoclonal antibodies to treat pSS and a number of clinical trials are in progress. This approach is already successfully in use for treating MALT lymphoma in pSS.
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20

Bowman, Simon, John Hamburger, Elizabeth Price, and Saaeha Rauz. Sjögren’s syndrome—clinical features. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0127_update_001.

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Abstract:
Sjögren’s syndrome is a chronic, immune-mediated, condition of unknown aetiology characterized by focal lymphocytic infiltration of exocrine glands associated with dry mouth and eyes. It occurs in its own right (primary Sjögren’s syndrome, pSS), or as a late feature of other rheumatic diseases such as rheumatoid arthritis, systemic lupus erythematosus or scleroderma (secondary Sjögren’s syndrome). There is a strong female bias. pSS typically affects women in their middle years with an estimated prevalence of 0.1–0.6%. 75% of patients have anti-Ro and/or anti-La antibodies, often with raised immunoglobulin levels (hypergammaglobulinaemia). In patients without these antibodies the diagnosis can be confirmed by salivary gland biopsy. Treatment is generally symptomatic using artificial tears, saliva replacements/stimulants and good dental hygiene. Three-quarters of patients with pSS report significant fatigue with a negative impact on quality of life. This can be the most disabling symptom. Approximately 20% of patients develop systemic features including persistent salivary gland swelling, cutaneous vasculitis, peripheral neuropathy, interstitial lung disease, autoimmune cytopenias or renal tubular acidosis. Hydroxychloroquine and corticosteroids are the most widely used therapies for systemic features. There is a 44fold increased risk of mucosa-associated lymphoid tissue (MALT) B-cell lymphoma in pSS, typically affecting the salivary glands. On account of abnormalities in the B-cell system in pSS there is current interest in the use of anti-B-cell directed monoclonal antibodies to treat pSS and a number of clinical trials are in progress. This approach is already successfully in use for treating MALT lymphoma in pSS.
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