Expansion of CD8+ T cells with regulatory function after interaction with intestinal epithelial cells

2002 ◽  
Vol 123 (5) ◽  
pp. 1516-1526 ◽  
Author(s):  
Matthieu Allez ◽  
Jens Brimnes ◽  
Iris Dotan ◽  
Lloyd Mayer
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Cd8 T Cells ◽  
Intestinal Epithelial Cells ◽  
Regulatory Function ◽  
Intestinal Epithelial

scholarly journals P010 GSDMB-mediated pyroptosis exacerbates intestinal inflammation by destroying intestinal epithelium in Crohn’s disease

2021 ◽  
Vol 15 (Supplement_1) ◽  
pp. S129-S131
Author(s):  
W Gong ◽  
P Liu ◽  
J Ren
Keyword(s):  
T Cells ◽  
Crohn’S Disease ◽  
Epithelial Cells ◽  
Intestinal Mucosa ◽  
Cd8 T Cells ◽  
Intestinal Inflammation ◽  
Disease Risk ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Epithelial Injury

Abstract Background Intestinal epithelial injury acts an essential role in the pathogenesis and development of Crohn’s disease (CD). Recent studies indicated that gasdermin D (GSDMD) mediated pyroptosis in intestinal epithelial cell (IEC) contributes to the epithelial injury during intestinal inflammation. However, how gasdermin B (GSDMB) mediated pyroptosis regulates intestinal epithelial injury in CD remains unknown. Methods We studied the characteristics of GSDMB mediated pyroptosis in CD patients and intestinal epithelial cells (Caco-2, HT-29 and primary IECs). The CD8+ T cells were extracted from intestinal mucosa of CD patients and health controls, and then co cultured with normal primary IECs to observe the pyroptosis of IECs. We further analyzed the CD8+ T cell subsets that promote pyroptosis in intestinal biopsies of CD patients. In addition, we screened out four single nucleotide polymorphism (SNP) of GSDMB that related to disease risk of CD in the public IBD exomes database (https://ibd.broadinstitute.org/), and investigated their effects on pyroptosis. Results GSDMB mediated pyroptosis was notably increased in intestinal mucosa of active human CD, and only existed in intestinal epithelial cells (Figure 1). Granzyme A (GrzA) initiated the killing results by the cleavage of GSDMB in intestinal epithelial cells, and interferon gamma (IFN-γ) up-regulated GSDMB expression in intestinal epithelial cells and promoted pyroptosis (Figure 2). GSDMB in primary IECs was significantly cleaved when co cultured with CD8+ T cells from active CD patients, while the phenomenon weakened a lot when GrzA in CD8+ T cells or GSDMB in epithelial cells was knocked down (Figure 3). We also found that IL26 possive CD8+ T cells were the main CD8+ T cells subsets secreting GrzA (Figure 3). We screened out two SNP of GSDMB related to increased disease risk of CD (rs2305480 and rs11078928) and two related to decreased disease risk (rs35104165 and rs143933205), and constructed these four mutant plasmids. Compared with wild type of GSDMB, rs2305480 promoted the cleavage while rs35104165 blocked the cleavage (Figure 4). Conclusion GSDMB-mediated pyroptosis results in intestinal epithelial injury, which will exacerbate intestinal inflammation. Modulation of the GSDMB-mediated pyroptosis emerges as a potential therapeutic strategy to target epithelium damage and treat CD.

Activation of a Unique Population of CD8+T Cells by Intestinal Epithelial Cells

2004 ◽  
Vol 1029 (1) ◽  
pp. 22-35 ◽  
Author(s):  
MATTHIEU ALLEZ ◽  
JENS BRIMNES ◽  
LING SHAO ◽  
IRIS DOTAN ◽  
ATSUSHI NAKAZAWA ◽  
...  
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Cd8 T Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial

scholarly journals Lymph-borne CD8α+ dendritic cells are uniquely able to cross-prime CD8+ T cells with antigen acquired from intestinal epithelial cells

2014 ◽  
Vol 8 (1) ◽  
pp. 38-48 ◽  
Author(s):  
V Cerovic ◽  
S A Houston ◽  
J Westlund ◽  
L Utriainen ◽  
E S Davison ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Epithelial Cells ◽  
Cd8 T Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial

scholarly journals Human CD8+ T Cells Clear Cryptosporidium parvum from Infected Intestinal Epithelial Cells

2010 ◽  
Vol 82 (4) ◽  
pp. 600-607 ◽  
Author(s):  
Birte Pantenburg ◽  
Honorine D. Ward ◽  
Sara M. Dann ◽  
Rhykka L. Connelly ◽  
Alejandro Castellanos-Gonzalez ◽  
...  
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Cryptosporidium Parvum ◽  
Cd8 T Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial

scholarly journals IL-17A Reprograms Intestinal Epithelial Cells to Facilitate HIV-1 Replication and Outgrowth in CD4+ T-cells

iScience ◽  
2021 ◽  
pp. 103225
Author(s):  
Tomas Raul Wiche Salinas ◽  
Annie Gosselin ◽  
Laurence Raymond Marchand ◽  
Etiene Moreira Gabriel ◽  
Olivier Tastet ◽  
...  
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Cd4 T Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Hiv 1

scholarly journals Human intestinal epithelial cell-induced CD8+ T cell activation is mediated through CD8 and the activation of CD8-associated p56lck.

1995 ◽  
Vol 182 (4) ◽  
pp. 1079-1088 ◽  
Author(s):  
Y Li ◽  
X Y Yio ◽  
L Mayer
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
T Cell ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
T Cell Activation ◽  
Cell Activation ◽  
Intestinal Epithelial Cells ◽  
T Cell Proliferation ◽  
Intestinal Epithelial

The activation of CD8+ suppressor T cells by normal intestinal epithelial cells in antigen-specific or allogeneic mixed cell culture systems has significant implications for the regulation of mucosal immune responses. In this study, we found that the capacity of epithelial cells to induce CD8+ suppressor T cell activation appeared to be linked to the binding of CD8 molecules on the T cell surface. This appears to be mediated by a non-class I molecule expressed on the epithelial cell surface, which binds to CD8 and results in the activation of the CD8-associated src-like tyrosine kinase, p56lck. Epithelial cell-stimulated p56lck activation is an early event (in contrast to monocytes) and is essential for T cell activation, since proliferation could be completely abrogated by pretreatment of T cells with genestein or herbamycin, both of which are protein tyrosine kinase inhibitors. Pretreatment of T cells with anti-CD8 or of intestinal epithelial cells with an anti-epithelial cell mAb B9 inhibited p56lck activation and further confirmed that CD8 on the T cell and a CD8 ligand on the epithelial cell were involved in this T cell activation event. The specificity of this reaction was confirmed in experiments in which murine transfectants 3G4 and 3G8, expressing CD4 or CD8, respectively, were used. Coculture of 3G8 with epithelial cells but not with monocytes activated p56lck in this cell line, whereas p56lck was preferentially activated in 3G4 cells when monocytes were used as the stimulator cells. Although stimulation through CD8- and CD8-associated p56lck was important for epithelial cell-induced T cell activation, T cell proliferation could not be induced by cross-linking CD8 alone with monoclonal antibody anti-CD8. These data suggest that a second signal, possibly through the T cell antigen receptor since activation of the T cell receptor-associated kinase fyn was also seen, is required for epithelial cell-driven T cell proliferation.

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