scholarly journals CD1d is involved in T cell-intestinal epithelial cell interactions.

1993 ◽  
Vol 178 (3) ◽  
pp. 1115-1119 ◽  
Author(s):  
A Panja ◽  
R S Blumberg ◽  
S P Balk ◽  
L Mayer
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
T Cell ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Cell Interactions ◽  
T Cell Proliferation ◽  
Intestinal Epithelial ◽  
No Inhibition

We assessed the role of the nonclassical class I molecule, CD1d, in the interaction between intestinal epithelial cells and T cells. In a mixed lymphocyte reaction (MLR) system where the stimulator cells were irradiated normal intestinal cells, the anti-CD1d monoclonal antibody (mAb) 3C11 inhibited T cell proliferation. In contrast, no inhibition was seen when mAb 3C11 was added to conventional MLR cultures (non T cell stimulators). Furthermore, no inhibition was seen when either airway epithelial cells were used as stimulator cells or lamina propria lymphocytes were used as responder cells. These latter two conditions along with a conventional MLR favor CD4+ T cell proliferation. However, we have previously shown that normal intestinal epithelial cells stimulate CD8+ T cells under similar culture conditions. Thus, CD1d expressed on intestinal epithelial cells may be an important ligand in CD8+ T cell-epithelial cell interactions.

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.

Induction of endothelin-1 synthesis by IL-2 and its modulation of rat intestinal epithelial cell growth

1998 ◽  
Vol 275 (3) ◽  
pp. G556-G563 ◽  
Author(s):  
Takeharu Shigematsu ◽  
Soichiro Miura ◽  
Masahiko Hirokawa ◽  
Ryota Hokari ◽  
Hajime Higuchi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Lines ◽  
Proliferative Response ◽  
Intestinal Epithelial Cell ◽  
Culture Media ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial

Endothelin (ET), a vasoconstrictive peptide, is known to have a variety of biological actions. Although ET is released by vascular endothelial cells, other cell populations also have been reported to synthesize and release ET. In this study, we examined whether ET is synthesized by intestinal epithelial cells and whether it affects induction of epithelial cell proliferation by interleukin-2 (IL-2). Subconfluent monolayers of intestinal epithelial cells (IEC-6 and IEC-18) were maintained in serum-free medium before addition of rat IL-2. Both IEC-6 and IEC-18 cells released ET-1 into the medium under unstimulated conditions, as determined by a sandwich ELISA. IL-2 significantly enhanced ET-1 release in a time-dependent manner. ET-3 was not detectable in the culture media of either cell line. Expression of ET-1 and ET-3 mRNA in epithelial cells was assessed by competitive PCR. Both cell lines were shown to express ET-1 mRNA, but no ET-3 mRNA was detected. IL-2 treatment enhanced ET-1 mRNA expression by both IEC-6 and IEC-18 cells. Both cell lines also expressed mRNA for ETA and ETB receptor subtypes. When cell proliferation was assessed, exogenous ET-1 induced a slight proliferative response in both types of cells that was consistent and significant at low ET-1 concentrations; cell growth was inhibited at a higher concentration (10−7M). IL-2 produced a significant proliferative response in both cell lines. However, the addition of ET-1 (10−7 M) to culture media attenuated the IL-2-induced increase in cell proliferation. ETA-receptor antagonists significantly enhanced cellular proliferation, suggesting involvement of the ETA receptor in modulation of IL-2-induced intestinal epithelial cell growth.

scholarly journals Regulated MIP-3α/CCL20 production by human intestinal epithelium: mechanism for modulating mucosal immunity

2001 ◽  
Vol 280 (4) ◽  
pp. G710-G719 ◽  
Author(s):  
Arash Izadpanah ◽  
Michael B. Dwinell ◽  
Lars Eckmann ◽  
Nissi M. Varki ◽  
Martin F. Kagnoff
Keyword(s):  
T Cells ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Intestinal Epithelium ◽  
Mucosal Immunity ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Adaptive Immune ◽  
Regulated Expression ◽  
Human Intestinal Epithelium

Human intestinal epithelial cells secrete an array of chemokines known to signal the trafficking of neutrophils and monocytes important in innate mucosal immunity. We hypothesized that intestinal epithelium may also have the capacity to play a role in signaling host adaptive immunity. The CC chemokine macrophage inflammatory protein (MIP)-3α/CCL20 is chemotactic for immature dendritic cells and CD45RO+T cells that are important components of the host adaptive immune system. In these studies, we demonstrate the widespread production and regulated expression of MIP-3α by human intestinal epithelium. Several intestinal epithelial cell lines were shown to constitutively express MIP-3α mRNA. Moreover, MIP-3α mRNA expression and protein production were upregulated by stimulation of intestinal epithelial cells with the proinflammatory cytokines tumor necrosis factor-α or interleukin-1α or in response to infection with the enteric bacterial pathogens Salmonella or enteroinvasive Escherichia coli. In addition, MIP-3α was shown to function as a nuclear factor-κB target gene. In vitro findings were paralleled in vivo by increased expression of MIP-3α in the epithelium of cytokine-stimulated or bacteria-infected human intestinal xenografts and in the epithelium of inflamed human colon. Mucosal T cells, other mucosal mononuclear cells, and intestinal epithelial cells expressed CCR6, the cognate receptor for MIP-3α. The constitutive and regulated expression of MIP-3α by human intestinal epithelium is consistent with a role for epithelial cell-produced MIP-3α in modulating mucosal adaptive immune responses.

scholarly journals PSIX-17 Investigating the biological activities of sodium cellobionate produced from cellulosic biomass

2020 ◽  
Vol 98 (Supplement_3) ◽  
pp. 187-187
Author(s):  
Lauren Kovanda ◽  
Zhiliang Fan ◽  
Xunde Li ◽  
Yanhong Liu
Keyword(s):  
Cell Proliferation ◽  
Antimicrobial Activity ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial Cells ◽  
Biological Activities ◽  
Radical Scavenging ◽  
Intestinal Epithelial

Abstract A novel method has been developed to easily hydrolyze cellulose to sodium cellobionate in a filamentous fungas, Neurospora crassa. The objectives of this experiment were to investigate the in vitro biological activities of sodium cellobionate. Antioxidant activity was evaluated with 3 chemical-based assays, including DPPH radical scavenging assay (DPPH), Trolox equivalent antioxidant capacity assay (TEAC), and ferric reducing antioxidant power assay (FRAP). Antimicrobial activity was determined as minimum inhibitory concentration (MIC) that prevented growth of tested bacteria, including four gram-negative bacteria (Escherichia coli F18 and ATCC 25922, and Salmonella Typhimurium ATCC 14028 and a wild strain isolated from cull diary cows in California) and one gram-positive bacteria (Enterococcus faecalis ATCC 29212). Anti-inflammatory activity was tested by analyzing TNF-α production with porcine alveolar macrophages that were challenged with lipopolysaccharide. A porcine intestinal epithelial cell line, IPEC-J2, was also used to test the effects of cellobionate on cell proliferation of intestinal epithelial cells. The tested doses of sodium cellobionate were 0, 0.04, 0.20, 1.00, 2.00, 4.00, 20.00, and 40.00 mg/mL. All assays were performed with over 6 replicates, except that MIC assays were performed as triplicate. All data were analyzed by PROC MIXED of SAS. Sodium cellobionate did not have radical scavenging capacity, but had weak FRAP (9.68 μM L-Cysteine equivalent) and TEAC (69% reduction) at the dose of 40 mg/mL. MIC results revealed that sodium cellobionate did not inhibit the growth of all tested bacteria, indicating it does not have antimicrobial activity within the range of tested doses. Sodium cellobionate did not exhibit anti-inflammatory activities, but significantly enhanced (P < 0.05) intestinal epithelial cell proliferation in vitro by 24.00%, 39.64%, and 25.98% when the doses were 1.00, 2.00, and 4.00 mg/mL, respectively. Results of this experiment indicate that cellobionate has limited biological activities in vitro, except that this biomass product could strongly stimulate the proliferation of intestinal epithelial cells. Future research will focus on the potential impacts of sodium cellobionate on intestinal physiology in vivo.

Human Follicular Dendritic Cells Inhibit Superantigen-Induced T-Cell Proliferation by Distinct Mechanisms

Blood ◽  
1999 ◽  
Vol 94 (1) ◽  
pp. 216-224 ◽  
Author(s):  
Anthony W. Butch ◽  
Kathleen A. Kelly ◽  
Michael S. Willbanks ◽  
Xinwen Yu
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Germinal Center ◽  
Cell Interactions ◽  
T Cell Proliferation ◽  
Cellular Interactions ◽  
Follicular Dendritic Cells ◽  
Follicular Dendritic

Follicular dendritic cells (FDCs) reside within germinal centers of secondary lymphoid tissue where they play a critical role in antigen-driven immune responses. FDCs express numerous adhesion molecules that facilitate cellular interactions with B and T cells within the germinal center microenvironment. Although human FDCs have been shown to influence B-cell development, very little is known about the ability of FDCs to regulate T-cell responses. To investigate this functional aspect of FDCs, highly enriched preparations were isolated by magnetic cell separation using the FDC-restricted monoclonal antibody HJ2. We found that isolated human FDCs inhibited proliferation of both autologous and allogeneic T cells, and were dependent on the number of FDCs present. Inhibition by FDCs was observed using two serologically distinct superantigens at multiple concentrations (Staphylococcus enterotoxin A and B). In contrast, B cells failed to inhibit, and often augmented superantigen-induced T-cell proliferation. Antibody-blocking studies showed that CD54 and CD106 were involved in the ability of FDC to inhibit T-cell proliferative responses. When FDCs and T cells were separated by a semipermeable membrane, the inhibitory effect was partially abrogated, demonstrating that in addition to cell-cell interactions, a soluble factor(s) was also involved in the process. The addition of indomethicin to cultures improved the proliferative response in the presence of FDCs, indicating that inhibition was mediated, in part, by prostaglandins. These results indicate that FDCs regulate T-cell proliferation by two molecular mechanisms and that FDC:T-cell interactions may play a pivotal role in germinal center development.

IL-10 modulates intestinal damage and epithelial cell apoptosis in T cell-mediated enteropathy

2004 ◽  
Vol 287 (3) ◽  
pp. G599-G604 ◽  
Author(s):  
Pengfei Zhou ◽  
Cathy Streutker ◽  
Rajka Borojevic ◽  
Yufa Wang ◽  
Ken Croitoru
Keyword(s):  
T Cell ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Apoptosis ◽  
Intestinal Epithelial Cells ◽  
Intestinal Damage ◽  
Intestinal Epithelial ◽  
Intestinal Tissue ◽  
Epithelial Cell Apoptosis

In vivo T cell activation by anti-CD3 monoclonal antibody (mAb) results in intestinal damage characterized by loss of villi and epithelial cell apoptosis. The role of the increased interleukin (IL)-10 released during this process is not clear. We assessed the effects of IL-10 on T cell-induced mucosal damage in vivo using IL-10-deficient C57BL/6 [IL-10 knockout (KO)] mice. IL-10 KO and wild-type C57BL/6 mice were injected with anti-CD3 mAb and observed for diarrhea. Changes in serum cytokine levels were measured by ELISA. Histological changes and epithelial cell apoptosis were analyzed on hematoxylin- and eosin-stained tissue sections. Fas expression on intestinal epithelial cells was assessed by flow cytometry analysis of freshly isolated intestinal epithelial cells. Anti-CD3-treated IL-10 KO mice developed more severe diarrhea, a greater loss of intestinal villi, and an increase in the numbers of apoptotic cells in the crypt epithelium. This difference in IL-10 KO mice was associated with an increase in serum tumor necrosis factor-α and interferon-γ levels and with an increase in Fas expression on fresh, isolated, small intestinal epithelial cells. In addition, the enhanced intestinal tissue damage induced by anti-CD3 in IL-10 KO mice was significantly diminished by treatment with recombinant murine IL-10. Therefore, the lack of IL-10 allowed for an increased T cell-induced intestinal tissue damage, and this was associated with an increase in T cell cytokine release and an increase in epithelial cell Fas expression.

scholarly journals Interleukin (IL)-22 from IL-20 Subfamily of Cytokines Induces Colonic Epithelial Cell Proliferation Predominantly through ERK1/2 Pathway

2019 ◽  
Vol 20 (14) ◽  
pp. 3468 ◽  
Author(s):  
Md. Moniruzzaman ◽  
Ran Wang ◽  
Varinder Jeet ◽  
Michael A. McGuckin ◽  
Sumaira Z. Hasnain
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Imaging System ◽  
Intestinal Epithelial Cells ◽  
Human Colon ◽  
Epithelial Cell Line ◽  
Intestinal Epithelial ◽  
Human Colon Cancer ◽  
Transcriptional Changes

The interleukin (IL)-20 subfamily of cytokines consists of IL-19, IL-20, IL-22, IL-24, and IL-26, and the expression of IL-20, IL-22, and IL-24 is reported to be higher in the colon of patients with ulcerative colitis. Although the receptors for these cytokines are highly expressed in the colon epithelium, their effects on epithelial renewal are not clearly understood. This study evaluated the effects of IL-20, IL-22, and IL-24 in epithelial renewal using the LS174T human colon cancer epithelial cell line. LS174T cells were treated with IL-20, IL-22, and IL-24 (25, 50, and 100 ng/mL) and a live-cell imaging system was used to evaluate the effects on cell proliferation. Following treatment, the signaling pathways contributing to cell proliferation were investigated through Western blotting in LS174T cells and downstream transcriptional changes through qRT-PCR in LS174T cells, and RNA-Seq in primary murine intestinal epithelial cells. Our results demonstrated that only IL-22 promoted LS174T cell proliferation, mediated via extracellular-signal-regulated kinase (ERK)1/2-mediated downstream regulation of p90RSK, c-Jun, and transcriptional changes of TRIM15 and STOM. IL-22 also promoted expression of ERK1/2-independent genes such as DDR2, LCN2, and LRG1, which are known to be involved in cell proliferation and migration. This study suggests that IL-22 induces cell proliferation in highly proliferative cells such as intestinal epithelial cells.

scholarly journals A Discrete Subpopulation of Dendritic Cells Transports Apoptotic Intestinal Epithelial Cells to T Cell Areas of Mesenteric Lymph Nodes

2000 ◽  
Vol 191 (3) ◽  
pp. 435-444 ◽  
Author(s):  
Fang-Ping Huang ◽  
Nicholas Platt ◽  
Michelle Wykes ◽  
James R. Major ◽  
Timothy J. Powell ◽  
...  
Keyword(s):  
T Cell ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Lymph Nodes ◽  
Intestinal Epithelial Cells ◽  
Nonspecific Esterase ◽  
Intestinal Epithelial ◽  
Mesenteric Lymph Nodes ◽  
Electrophoretic Variants ◽  
Mesenteric Lymph

This study identifies a dendritic cell (DC) subset that constitutively transports apoptotic intestinal epithelial cell remnants to T cell areas of mesenteric lymph nodes in vivo. Rat intestinal lymph contains two DC populations. Both populations have typical DC morphology, are major histocompatibility complex class IIhi, and express OX62, CD11c, and B7. CD4+/OX41+ DCs are strong antigen-presenting cells (APCs). CD4−/OX41− DCs are weak APCs and contain cytoplasmic apoptotic DNA, epithelial cell–restricted cytokeratins, and nonspecific esterase (NSE)+ inclusions, not seen in OX41+ DCs. Identical patterns of NSE electrophoretic variants exist in CD4−/OX41− DCs, intestinal epithelial cells, and mesenteric node DCs but not in other DC populations, macrophages, or tissues. Terminal deoxynucleotidyl transferase–mediated dUTP-biotin nick-end labeling (TUNEL)-positive DCs and strongly NSE+ DCs are present in intestinal lamina propria. Peyer's patches and mesenteric but not other lymph nodes contain many strongly NSE+ DCs in interfollicular and T cell areas. Similar DCs are seen in the ileum and in T cell areas of mesenteric nodes in gnotobiotic rats. These results show that a distinct DC subset constitutively endocytoses and transports apoptotic cells to T cell areas and suggest a role for these DCs in inducing and maintaining peripheral self-tolerance.

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