Intestinal epithelial cells (IECs) from IBD patients preferentially stimulate IFN-γ production by CD4+ T cells

2001 ◽  
Vol 120 (5) ◽  
pp. A321
Author(s):  
Iris Dotan ◽  
Lloyd Mayer
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Cd4 T Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Ifn Γ

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 Salmonella entericaSerovar Typhimurium Increases Functional PD-L1 Synergistically with Gamma Interferon in Intestinal Epithelial Cells viaSalmonellaPathogenicity Island 2

2018 ◽  
Vol 86 (5) ◽  
pp. e00674-17 ◽  
Author(s):  
J. M. Sahler ◽  
C. R. Eade ◽  
C. Altier ◽  
J. C. March
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Host Cell ◽  
Immune Evasion ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Activated T Cells ◽  
Content Type ◽  
Ifn Γ ◽  
First Time

ABSTRACTNontyphoidal serovars ofSalmonella entericaare pathogenic bacteria that are common causes of food poisoning. WhereasSalmonellamechanisms of host cell invasion, inflammation, and pathogenesis are mostly well established, a new possible mechanism of immune evasion is being uncovered. Programmed death ligand 1 (PD-L1) is an immunosuppressive membrane protein that binds to activated T cells via their PD-1 receptor and thereby halts their activation. PD-L1 expression plays an essential role in the immunological tolerance of self-antigens but is also exploited for immune evasion by pathogen-infected cells and cancer cells. Here, we show for the first time thatSalmonellainfection of intestinal epithelial cells causes the induction of PD-L1. The increased expression of PD-L1 throughSalmonellainfection was seen in both human and rat intestinal epithelial cell lines. We determined that cellular invasion by the bacteria is necessary for PD-L1 induction, potentially indicating thatSalmonellastrains are delivering mediators from inside the host cell that trigger the increased PD-L1 expression. Using knockout mutants, we determined that this effect largely originates from theSalmonellapathogenicity island 2. We also show for the first time in any cell type thatSalmonellacombined with gamma interferon (IFN-γ) causes a synergistic induction of PD-L1. Finally, we show thatSalmonellaplus IFN-γ induction of PD-L1 decreased the cytokine production of activated T cells. UnderstandingSalmonellaimmune evasion strategies could generate new therapeutic targets and help to manipulate PD-L1 expression in other diseases.

scholarly journals IL-17A imprints intestinal epithelial cells with the ability to promote HIV-1 dissemination/outgrowth in CD4 T cells

2019 ◽  
Vol 5 ◽  
pp. 20-21
Author(s):  
T. Wiche Salinas ◽  
A. Gosselin ◽  
B. Mariana ◽  
H. Touil ◽  
Y. Zhang ◽  
...  
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Cd4 T Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Hiv 1

scholarly journals Exposure of Intestinal Epithelial Cells to 2′-Fucosyllactose and CpG Enhances Galectin Release and Instructs Dendritic Cells to Drive Th1 and Regulatory-Type Immune Development

Biomolecules ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 784 ◽  
Author(s):  
Veronica Ayechu-Muruzabal ◽  
Saskia A. Overbeek ◽  
Atanaska I. Kostadinova ◽  
Bernd Stahl ◽  
Johan Garssen ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Epithelial Cells ◽  
Cd4 T Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Cpg Dna ◽  
Immune Development ◽  
Adaptive Immune Cells ◽  
Tgf Β1

Intestinal epithelial cells (IEC) release immunomodulatory galectins upon exposure to CpG DNA (mimicking bacterial triggers) and short-chain galacto- and long-chain fructo-oligosaccharides (GF). This study aims to investigate the immunomodulatory properties of 2′-fucosyllactose (2′-FL), a non-digestible oligosaccharide (NDO) abundantly present in human milk, using a co-culture model developed to study the crosstalk between IEC and innate and adaptive immune cells. IECs, co-cultured with αCD3/CD28-activated peripheral blood mononuclear cells (PBMC), were apically exposed to NDOs and CpG, washed and co-cultured with immature monocyte-derived dendritic cells (moDC). Subsequently, moDC were co-cultured with naïve CD4+ T-cells. In the presence of CpG, both 2′-FL or GF-exposed IEC enhanced Th1-type IFNγ and regulatory IL-10 secretion of PBMCs, compared to CpG alone, while Th2-type IL-13 was reduced. Both NDOs increased IEC-derived galectin-3, -4, -9 and TGF-β1 of CpG-exposed IEC. Only galectin-9 correlated with all modified immune parameters and TGF-β1 secretion. MoDCs exposed to 2′-FL and CpG-conditioned IEC instructed IFNγ and IL-10 secretion by CD4+ T-cells, suggesting the development of a regulatory Th1 response. These results reveal that 2′-FL and GF could contribute to the mucosal immune development by supporting the effect of microbial CpG DNA associated with the modulation of epithelial galectin and TGF-β1 secretion.

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