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Immunology for University Students
Resources and Material for Lecturers and Students - Immunology (University level)
Curated by Alfredo Corell
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Partial Sleep Restriction Activates Immune Response-Related Gene Expression Pathways: Experimental and Epidemiological Studies in Humans

Partial Sleep Restriction Activates Immune Response-Related Gene Expression Pathways: Experimental and Epidemiological Studies in Humans | Immunology for University Students | Scoop.it
PLOS ONE: an inclusive, peer-reviewed, open-access resource from the PUBLIC LIBRARY OF SCIENCE. Reports of well-performed scientific studies from all disciplines freely available to the whole world.
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Epidemiological studies have shown that short or insufficient sleep is associated with increased risk for metabolic diseases and mortality. To elucidate mechanisms behind this connection, we aimed to identify genes and pathways affected by experimentally induced, partial sleep restriction and to verify their connection to insufficient sleep at population level. The experimental design simulated sleep restriction during a working week: sleep of healthy men (N = 9) was restricted to 4 h/night for five nights. The control subjects (N = 4) spent 8 h/night in bed. Leukocyte RNA expression was analyzed at baseline, after sleep restriction, and after recovery using whole genome microarrays complemented with pathway and transcription factor analysis. Expression levels of the ten most up-regulated and ten most down-regulated transcripts were correlated with subjective assessment of insufficient sleep in a population cohort (N = 472). Experimental sleep restriction altered the expression of 117 genes. Eight of the 25 most up-regulated transcripts were related to immune function. Accordingly, fifteen of the 25 most up-regulated Gene Ontology pathways were also related to immune function, including those for B cell activation, interleukin 8 production, and NF-κB signaling (P<0.005). Of the ten most up-regulated genes, expression of STX16 correlated negatively with self-reported insufficient sleep in a population sample, while three other genes showed tendency for positive correlation. Of the ten most down-regulated genes, TBX21 andLGR6 correlated negatively and TGFBR3 positively with insufficient sleep. Partial sleep restriction affects the regulation of signaling pathways related to the immune system. Some of these changes appear to be long-lasting and may at least partly explain how prolonged sleep restriction can contribute to inflammation-associated pathological states, such as cardiometabolic diseases.

  
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Role of the gut microbiota in immunity and inflammatory disease

Role of the gut microbiota in immunity and inflammatory disease | Immunology for University Students | Scoop.it
This month's featured article is on the intestinal microbiota: http://t.co/giUTDnF2sU
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Nature Reviews Immunology 13, 321-335 (May 2013) | doi:10.1038/nri3430

Role of the gut microbiota in immunity and inflammatory disease

Nobuhiko Kamada1, Sang-Uk Seo1, Grace Y. Chen2 & Gabriel Núñez

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Fat's Immune Sentinels | The Scientist Magazine®

Fat's Immune Sentinels | The Scientist Magazine® | Immunology for University Students | Scoop.it

Fat's Immune Sentinels

Certain immune cells keep adipose tissue in check by helping to define normal and abnormal physiological states.

By Justin Odegaard and Ajay Chawla | December 1, 2012

 

Obesity and associated health consequences are the greatest public-health challenges of our time. Worldwide, an estimated 1.5 billion people tip the scales as overweight—300–500 million of whom are obese—placing nearly a quarter of humanity at dramatically increased risk for diabetes, cardiovascular disease, and many types of cancer. While considerable scientific investments have barely begun to slow the expansion of our waistlines, they have yielded unexpected physiologic insights, perhaps the greatest of which is the discovery that proper metabolic function requires a previously unsuspected level of cooperation between the cells that make up each internal organ and that organ’s resident leukocytes.

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Sky Sirewest's curator insight, November 15, 2013 2:38 AM

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Two new Inmune animations: Inflammation

http://www.facebook.com/ArmandoHasudungan
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Again a drawing and explanation by Armando Hasudungan. In this ocasion about Inflammation

 

Link to the part II: http://www.youtube.com/watch?v=aD6UD1ETMCg&list=TL4MCqoFYTScY

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Natural killer cells help to tolerate fetus during pregnacy by regulating inflammatory TH17 cells at the maternal-fetal interface

Natural killer cells help to tolerate fetus during pregnacy by regulating inflammatory TH17 cells at the maternal-fetal interface | Immunology for University Students | Scoop.it
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Binqing Fua,Xianchang Lib,c,Rui Suna,Xianhong Tongd,Bin Lingd,Zhigang Tiana,1, andHaiming Weia,1

 

Natural killer (NK) cells accumulate at the maternal–fetal interface in large numbers, but their exact roles in successful pregnancy remain poorly defined. Here, we provide evidence that TH17 cells and local inflammation can occur at the maternal–fetal interface during natural allogenic pregnancies. We found that decidual NK cells promote immune tolerance and successful pregnancy by dampening inflammatory TH17 cells via IFN-γ secreted by the CD56brightCD27+ NK subset. This NK-cell–mediated regulatory response is lost in patients who experience recurrent spontaneous abortions, which results in a prominent TH17 response and extensive local inflammation. This local inflammatory response further affects the regulatory function of NK cells, leading to the eventual loss of maternal-fetal tolerance. Thus, our data identify NK cells as key regulatory cells at the maternal–fetal interface by suppressing TH17-mediated local inflammation.

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