Tu1672 IL-21 Production and Function in Peripheral Immune Cells From Crohn's Disease Patients

2013 ◽  
Vol 144 (5) ◽  
pp. S-819
Author(s):  
Jennifer H. Cox ◽  
Evan Thomas ◽  
Rebecca P. Wu ◽  
Kem Valliant-Saunders ◽  
Scott Hussell ◽  
...  
Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 813
Author(s):  
Laurence Chapuy ◽  
Marika Sarfati

Inflammatory bowel diseases (IBDs), which include Crohn’s disease (CD) and ulcerative colitis (UC), are driven by an abnormal immune response to commensal microbiota in genetically susceptible hosts. In addition to epithelial and stromal cells, innate and adaptive immune systems are both involved in IBD immunopathogenesis. Given the advances driven by single-cell technologies, we here reviewed the immune landscape and function of mononuclear phagocytes in inflamed non-lymphoid and lymphoid tissues of CD and UC patients. Immune cell profiling of IBD tissues using scRNA sequencing combined with multi-color cytometry analysis identifies unique clusters of monocyte-like cells, macrophages, and dendritic cells. These clusters reflect either distinct cell lineages (nature), or distinct or intermediate cell types with identical ontogeny, adapting their phenotype and function to the surrounding milieu (nurture and tissue imprinting). These advanced technologies will provide an unprecedented view of immune cell networks in health and disease, and thus may offer a personalized medicine approach to patients with IBD.


2019 ◽  
Vol 13 (Supplement_1) ◽  
pp. S092-S092
Author(s):  
P Harrow ◽  
R Datta ◽  
A Stagg ◽  
J O Lindsay

2014 ◽  
Vol 146 (5) ◽  
pp. S-649
Author(s):  
Z. Gordon Jiang ◽  
Alan C. Moss ◽  
Vilmosne G. Csizmadia ◽  
Adam S. Cheifetz ◽  
Yan Wu ◽  
...  

2010 ◽  
Vol 17 (6) ◽  
pp. 526-531 ◽  
Author(s):  
G Sivaram ◽  
Santosh K Tiwari ◽  
Avinash Bardia ◽  
G Manoj ◽  
B Santhosh ◽  
...  

2017 ◽  
Vol 152 (5) ◽  
pp. S764
Author(s):  
Jakob B. Seidelin ◽  
Amani Younis ◽  
Ole H. Nielsen

2001 ◽  
Vol 60 (3) ◽  
pp. 365-374 ◽  
Author(s):  
Caroline M. Pond

Redistribution of white adipose tissue is a long-term symptom of several chronic diseases. Although the roles of adipocytes in acute illness have been thoroughly studied, how or why short-term responses of adipose tissue to disease sometimes produce long-term redistribution, and the causal relationship between the anatomical changes and the associated metabolic syndromes are poorly understood. The present paper reviews explanations for the redistribution of adipose tissue after infection with HIV, and in Crohn's disease; both conditions that share the peculiarity of selective expansion of certain adipose depots while others are depleted. HIV adipose tissue redistribution syndrome (HARS) develops gradually after several months of infection with the HIV both in untreated patients and in those taking protease inhibitors and nucleoside reverse transcriptase inhibitors. Some current theories about the causes of HARS are critically assessed, and reasons presented for implicating local interactions between the immune system and perinodal adipocytes. Some evolutionary aspects of conspicuous long-term changes in the distribution of human adipose tissue are discussed. Adipose tissue acts as a social signal, indicating dietary history and previous exposure to pathogens. A distinctive symptom of Crohn's disease is selective enlargement of the mesenteric adipose tissue near the diseased lymph nodes and intestine. Perinodal adipocytes have site-specific properties not found in adipocytes from nodeless depots, such as perirenal and epididymal, that may equip them to interact locally with lymph-node lymphoid cells, making polyunsaturated fatty acids selectively and rapidly available to activated immune cells. Studies of the time course of activation of perinodal adipocytes via the lymph nodes they enclose indicate that prolonged or frequent stimulation recruits more adipocytes to control by immune cells, which may lead to selective enlargement of node-containing depots. These concepts suggest hypotheses about HARS and the anomalous development of mesenteric adipose tissue in Crohn's disease that could form the basis for further investigations.


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