IMMUNOLOGICAL ASPECTS OF CROHN'S DISEASE: A REGULATORY FUNCTION OF TIM-3/GALECTIN-9 IN LYTH1.

Angelo Leone, Sabrina David, Francesco Carini, Francesca Rappa, Giovanni Tomasello, Margherita Mazzola, Raymond Zerbe, Abdo Jurjus

Risultato della ricerca: Article

Abstract

Crohn's disease (CD) is a type of inflammatory bowel disease (IBD) and its etiology is multifactorial and involves a combination of genetic environmental factors. The interaction of these factors causes an imbalance of the microbiota, leading to the activation of several immunological and inflammatory mechanism. From an immunological point of view, there seems to be an involvement of the TIM-3/GALECTIN-9 pathway and of the autoregulation of lyTh1. These studies show that in patients with CD the autoregulation of lyth1 is lost due to a reduced concentration of galectin-9 and a reduced TIM-3 expression in LyTh1. This could be one of the reason for the state of perpetual activation of lyTh1, resulting in the chronic inflammation process.
Lingua originaleEnglish
pagine (da-a)66-68
Numero di pagine3
RivistaDefault journal
Volume12
Stato di pubblicazionePublished - 2017

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Galectin 3
Crohn Disease
Homeostasis
Galectins
Microbiota
Inflammatory Bowel Diseases
Inflammation

All Science Journal Classification (ASJC) codes

  • Medicine(all)

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title = "IMMUNOLOGICAL ASPECTS OF CROHN'S DISEASE: A REGULATORY FUNCTION OF TIM-3/GALECTIN-9 IN LYTH1.",
abstract = "Crohn's disease (CD) is a type of inflammatory bowel disease (IBD) and its etiology is multifactorial and involves a combination of genetic environmental factors. The interaction of these factors causes an imbalance of the microbiota, leading to the activation of several immunological and inflammatory mechanism. From an immunological point of view, there seems to be an involvement of the TIM-3/GALECTIN-9 pathway and of the autoregulation of lyTh1. These studies show that in patients with CD the autoregulation of lyth1 is lost due to a reduced concentration of galectin-9 and a reduced TIM-3 expression in LyTh1. This could be one of the reason for the state of perpetual activation of lyTh1, resulting in the chronic inflammation process.",
author = "Angelo Leone and Sabrina David and Francesco Carini and Francesca Rappa and Giovanni Tomasello and Margherita Mazzola and Raymond Zerbe and Abdo Jurjus",
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AU - Leone, Angelo

AU - David, Sabrina

AU - Carini, Francesco

AU - Rappa, Francesca

AU - Tomasello, Giovanni

AU - Mazzola, Margherita

AU - Zerbe, Raymond

AU - Jurjus, Abdo

PY - 2017

Y1 - 2017

N2 - Crohn's disease (CD) is a type of inflammatory bowel disease (IBD) and its etiology is multifactorial and involves a combination of genetic environmental factors. The interaction of these factors causes an imbalance of the microbiota, leading to the activation of several immunological and inflammatory mechanism. From an immunological point of view, there seems to be an involvement of the TIM-3/GALECTIN-9 pathway and of the autoregulation of lyTh1. These studies show that in patients with CD the autoregulation of lyth1 is lost due to a reduced concentration of galectin-9 and a reduced TIM-3 expression in LyTh1. This could be one of the reason for the state of perpetual activation of lyTh1, resulting in the chronic inflammation process.

AB - Crohn's disease (CD) is a type of inflammatory bowel disease (IBD) and its etiology is multifactorial and involves a combination of genetic environmental factors. The interaction of these factors causes an imbalance of the microbiota, leading to the activation of several immunological and inflammatory mechanism. From an immunological point of view, there seems to be an involvement of the TIM-3/GALECTIN-9 pathway and of the autoregulation of lyTh1. These studies show that in patients with CD the autoregulation of lyth1 is lost due to a reduced concentration of galectin-9 and a reduced TIM-3 expression in LyTh1. This could be one of the reason for the state of perpetual activation of lyTh1, resulting in the chronic inflammation process.

UR - http://hdl.handle.net/10447/234546

M3 - Article

VL - 12

SP - 66

EP - 68

JO - Default journal

JF - Default journal

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