scholarly journals Membrane Vesicles Released by Intestinal Epithelial Cells Infected with Rotavirus Inhibit T-Cell Function

2010 ◽  
Vol 23 (6) ◽  
pp. 595-608 ◽  
Author(s):  
Alfonso Barreto ◽  
Luz-Stella Rodríguez ◽  
Olga Lucía Rojas ◽  
Marie Wolf ◽  
Harry B. Greenberg ◽  
...  
Keyword(s):  
T Cell ◽  
Epithelial Cells ◽  
Cell Function ◽  
Intestinal Epithelial Cells ◽  
Membrane Vesicles ◽  
Intestinal Epithelial ◽  
T Cell Function

Regulated production of interferon-inducible T-cell chemoattractants by human intestinal epithelial cells

2001 ◽  
Vol 120 (1) ◽  
pp. 49-59 ◽  
Author(s):  
Michael B. Dwinell ◽  
Norbert Lügering ◽  
Lars Eckmann ◽  
Martin F. Kagnoff
Keyword(s):  
T Cell ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Human Intestinal Epithelial Cells

scholarly journals Amelioration of Congenital Tufting Enteropathy in EpCAM (TROP1)-Deficient Mice via Heterotopic Expression of TROP2 in Intestinal Epithelial Cells

Cells ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 1847
Author(s):  
Gaku Nakato ◽  
Sohshi Morimura ◽  
Michael Lu ◽  
Xu Feng ◽  
Chuanjin Wu ◽  
...  
Keyword(s):  
Stem Cell ◽  
Epithelial Cells ◽  
Cell Function ◽  
Intestinal Epithelial Cells ◽  
Surface Proteins ◽  
Stem Cell Markers ◽  
Intestinal Epithelial ◽  
Mesenteric Lymph Nodes ◽  
Function Expression ◽  
Deficient Mice

TROP1 (EpCAM) and TROP2 are homologous cell surface proteins that are widely expressed, and often co-expressed, in developing and adult epithelia. Various functions have been ascribed to EpCAM and TROP2, but responsible mechanisms are incompletely characterized and functional equivalence has not been examined. Adult intestinal epithelial cells (IEC) express high levels of EpCAM, while TROP2 is not expressed. EpCAM deficiency causes congenital tufting enteropathy (CTE) in humans and a corresponding lethal condition in mice. We expressed TROP2 and EpCAM in the IEC of EpCAM-deficient mice utilizing a villin promoter to assess EpCAM and TROP2 function. Expression of EpCAM or TROP2 in the IEC of EpCAM knockout mice prevented CTE. TROP2 rescue (T2R) mice were smaller than controls, while EpCAM rescue (EpR) mice were not. Abnormalities were observed in the diameters and histology of T2R small intestine, and Paneth and stem cell markers were decreased. T2R mice also exhibited enlarged mesenteric lymph nodes, enhanced permeability to 4 kDa FITC-dextran and increased sensitivity to detergent-induced colitis, consistent with compromised barrier function. Studies of IEC organoids and spheroids revealed that stem cell function was also compromised in T2R mice. We conclude that EpCAM and TROP2 exhibit functional redundancy, but they are not equivalent.

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.

Oral tolerance to haptens: intestinal epithelial cells from 2,4-dinitrochlorobenzene-fed mice inhibit hapten-specific T cell activationin vitro

1995 ◽  
Vol 25 (5) ◽  
pp. 1385-1390 ◽  
Author(s):  
Veronique Galliaerde ◽  
Cyril Desvignes ◽  
Eric Peyron ◽  
Dominique Kaiserlian
Keyword(s):  
T Cell ◽  
Epithelial Cells ◽  
Oral Tolerance ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial

scholarly journals Mitochondrial complex II in intestinal epithelial cells regulates T cell-mediated immunopathology

2021 ◽  
Author(s):  
Hideaki Fujiwara ◽  
Keisuke Seike ◽  
Michael D. Brooks ◽  
Anna V. Mathew ◽  
Ilya Kovalenko ◽  
...  
Keyword(s):  
T Cell ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Mitochondrial Complex ◽  
Complex Ii

scholarly journals Endocytosis of commensal antigens by intestinal epithelial cells regulates mucosal T cell homeostasis

Science ◽  
2019 ◽  
Vol 363 (6431) ◽  
pp. eaat4042 ◽  
Author(s):  
Mark S. Ladinsky ◽  
Leandro P. Araujo ◽  
Xiao Zhang ◽  
John Veltri ◽  
Marta Galan-Diez ◽  
...  
Keyword(s):  
T Cell ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Commensal Bacteria ◽  
Dependent Manner ◽  
Intestinal Epithelial ◽  
T Helper 17 ◽  
Associated Proteins ◽  
Gut Microbe

Commensal bacteria influence host physiology, without invading host tissues. We show that proteins from segmented filamentous bacteria (SFB) are transferred into intestinal epithelial cells (IECs) through adhesion-directed endocytosis that is distinct from the clathrin-dependent endocytosis of invasive pathogens. This process transfers microbial cell wall–associated proteins, including an antigen that stimulates mucosal T helper 17 (TH17) cell differentiation, into the cytosol of IECs in a cell division control protein 42 homolog (CDC42)–dependent manner. Removal of CDC42 activity in vivo led to disruption of endocytosis induced by SFB and decreased epithelial antigen acquisition, with consequent loss of mucosal TH17 cells. Our findings demonstrate direct communication between a resident gut microbe and the host and show that under physiological conditions, IECs acquire antigens from commensal bacteria for generation of T cell responses to the resident microbiota.

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