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 ◽  
...  
2019 ◽  
Vol 5 ◽  
pp. 20-21
Author(s):  
T. Wiche Salinas ◽  
A. Gosselin ◽  
B. Mariana ◽  
H. Touil ◽  
Y. Zhang ◽  
...  

Biomolecules ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 784 ◽  
Author(s):  
Veronica Ayechu-Muruzabal ◽  
Saskia A. Overbeek ◽  
Atanaska I. Kostadinova ◽  
Bernd Stahl ◽  
Johan Garssen ◽  
...  

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.


2002 ◽  
Vol 8 (2) ◽  
pp. 150-156 ◽  
Author(s):  
Gang Meng ◽  
Xiping Wei ◽  
Xiaoyun Wu ◽  
Marty T. Sellers ◽  
Julie M. Decker ◽  
...  

Author(s):  
Yen-Hung Chow ◽  
Duan Yu ◽  
Jun-ying Zhang ◽  
Yiming Xie ◽  
O. Lu-Chen Wei ◽  
...  
Keyword(s):  
T Cells ◽  

1995 ◽  
Vol 182 (4) ◽  
pp. 1079-1088 ◽  
Author(s):  
Y Li ◽  
X Y Yio ◽  
L Mayer

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.


Sign in / Sign up

Export Citation Format

Share Document