scholarly journals Faculty Opinions recommendation of The transcription factor T-bet regulates mucosal T cell activation in experimental colitis and Crohn's disease.

2002 ◽  
Author(s):  
Steve Ward
Keyword(s):  
Transcription Factor ◽  
Crohn’S Disease ◽  
T Cell ◽  
Crohn's Disease ◽  
T Cell Activation ◽  
Cell Activation ◽  
Experimental Colitis

Inhibitor of interleukin-1? and interleukin-1?-induced T-cell activation in serum of patients with active Crohn's disease

1991 ◽  
Vol 36 (6) ◽  
pp. 737-742 ◽  
Author(s):  
J�rn Brynskov ◽  
Morten Bagge Hansen ◽  
Claus Reimert ◽  
Klaus Bendtzen
Keyword(s):  
Crohn’S Disease ◽  
T Cell ◽  
Crohn's Disease ◽  
T Cell Activation ◽  
Cell Activation ◽  
Interleukin 1

scholarly journals Impairment of CD4+ T and Memory B Cell Responses but Normal Memory CD8+T-Cell Activation on Crohn’s Disease after COVID-19 Vaccination: A Twin Case

Viruses ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2143
Author(s):  
Fabiana Gil Melgaço ◽  
Tamiris Azamor ◽  
Livia Melo Villar ◽  
Ana Paula Dinis Ano Bom ◽  
Juliana Gil Melgaço
Keyword(s):  
Crohn’S Disease ◽  
T Cell ◽  
Crohn's Disease ◽  
T Cell Activation ◽  
Cell Activation ◽  
Disease Patient ◽  
Antibody Detection ◽  
Cell Responses ◽  
Cell Immunity ◽  
The Impact

Vaccines to prevent the impact of SARS-CoV-2 are now available, including for patients with autoimmune diseases. However, there is no information about how inflammatory bowel disease (IBD) treatment could impact the cellular and humoral immune responses. This study evaluated SARS-CoV-2-specific humoral and cellular responses after vaccination with a two-dose schedule in a Crohn’s disease patient treated with Infliximab (10 mg/kg); we included comparisons with a monozygotic twin. The results showed that the Crohn’s disease’s twin (twin 2) had no antibody detection and reduced activation of CD4+ T cell responses, unlike the twin without the autoimmune disease (twin 1). Twin 2 developed antigen-specific central memory CD8+ T-cells and IFNγ production after the second dose of COVID-19 vaccination, similar to twin 1. These findings elucidated the role of T-cell immunity after COVID-19 immunization on IBD patients despite the lack of antibody production. Finally, our observation supports the consensus recommendation for IBD patients to receive COVID-19 vaccines.

T-cell activation in Crohn's disease

1990 ◽  
Vol 98 (3) ◽  
pp. 639-646 ◽  
Author(s):  
Ch. Mueller ◽  
P. Knoflach ◽  
C.C. Zielinski
Keyword(s):  
Crohn’S Disease ◽  
T Cell ◽  
Crohn's Disease ◽  
T Cell Activation ◽  
Cell Activation

scholarly journals Integrated Bioinformatics Analysis Identifies ELAVL1 and APP as Candidate Crucial Genes for Crohn’s Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-20
Author(s):  
Heli Li ◽  
Qianru Li ◽  
Shiran Sun ◽  
Ping Lei ◽  
Xiong Cai ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
T Cell ◽  
Crohn's Disease ◽  
Signaling Pathway ◽  
T Cell Activation ◽  
Peripheral Blood ◽  
Cell Activation ◽  
Mapk Signaling ◽  
Gene Set Enrichment Analysis ◽  
Infliximab Treatment

Immune imbalance and barrier destruction of intestinal mucosa are the central pathogenic factors of Crohn’s disease (CD). In this study, three independent microarray studies of CD were integrated and 9912 differentially expressed genes (DEGs) were analysed by NetworkAnalyst to screen candidate crucial genes. NetworkAnalyst identified ELAV-like RNA binding protein 1 (ELAVL1) as the most crucial upregulated gene and amyloid-β precursor protein (APP) as the most crucial downregulated gene in peripheral blood of CD patients. By computing significance with hypergeometric test based on the KEGG pathway database, upregulated DEGs highlight the pathways of T cell receptor signaling and the differentiation of T helpers. Downregulated DEGs were found enriched in pathways in multiple cancers, MAPK signaling, Rap1 signaling, and PI3K-AKT signaling. Further taking all DEGs together, Gene Set Enrichment Analysis (GSEA) brought out the NOD-like receptor (NLR) signaling pathway which could be regulated by ELAVL1. xCell found decreased naïve and differentiated T cell proportions in the peripheral blood of CD patients suggesting T cell migration to the intestinal tissue and/or exhaustion. Further, ELAVL1 expression correlating with multiple T cell proportions suggests that ELAVL1 may regulate T cell activation. These findings illustrated that ELAVL1 and APP were candidate crucial genes in the peripheral blood of CD patients. ELAVL1 possibly acts as a key regulator of T cell activation via the NLR signaling pathway. APP might be a downstream effector of infliximab treatment connecting with MAPK signaling.

scholarly journals The transcription factor NFATc2 controls IL-6–dependent T cell activation in experimental colitis

2008 ◽  
Vol 205 (9) ◽  
pp. 2099-2110 ◽  
Author(s):  
Benno Weigmann ◽  
Hans A. Lehr ◽  
George Yancopoulos ◽  
David Valenzuela ◽  
Andrew Murphy ◽  
...  
Keyword(s):  
T Cells ◽  
Transcription Factor ◽  
T Cell ◽  
T Lymphocytes ◽  
T Cell Activation ◽  
Cell Activation ◽  
Experimental Colitis ◽  
Regulatory Role ◽  
Dependent Manner ◽  
Chronic Intestinal Inflammation

The nuclear factor of activated T cells (NFAT) family of transcription factors controls calcium signaling in T lymphocytes. In this study, we have identified a crucial regulatory role of the transcription factor NFATc2 in T cell–dependent experimental colitis. Similar to ulcerative colitis in humans, the expression of NFATc2 was up-regulated in oxazolone-induced chronic intestinal inflammation. Furthermore, NFATc2 deficiency suppressed colitis induced by oxazolone administration. This finding was associated with enhanced T cell apoptosis in the lamina propria and strikingly reduced production of IL-6, -13, and -17 by mucosal T lymphocytes. Further studies using knockout mice showed that IL-6, rather than IL-23 and -17, are essential for oxazolone colitis induction. Administration of hyper-IL-6 blocked the protective effects of NFATc2 deficiency in experimental colitis, suggesting that IL-6 signal transduction plays a major pathogenic role in vivo. Finally, adoptive transfer of IL-6 and wild-type T cells demonstrated that oxazolone colitis is critically dependent on IL-6 production by T cells. Collectively, these results define a unique regulatory role for NFATc2 in colitis by controlling mucosal T cell activation in an IL-6–dependent manner. NFATc2 in T cells thus emerges as a potentially new therapeutic target for inflammatory bowel diseases.

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