scholarly journals Impairment of intestinal intraepithelial lymphocytes in Id2 deficient mice

Gut ◽  
2004 ◽  
Vol 53 (4) ◽  
pp. 480-486 ◽  
Author(s):  
J-K Kim
Keyword(s):  
Intraepithelial Lymphocytes ◽  
Intestinal Intraepithelial Lymphocytes ◽  
Deficient Mice

Altered development of intestinal intraepithelial lymphocytes in P-glycoprotein-deficient mice

2000 ◽  
Vol 24 (8) ◽  
pp. 783-795 ◽  
Author(s):  
Michael D Eisenbraun ◽  
R.Lee Mosley ◽  
Daniel H Teitelbaum ◽  
Richard A Miller
Keyword(s):  
Intraepithelial Lymphocytes ◽  
Intestinal Intraepithelial Lymphocytes ◽  
P Glycoprotein ◽  
Deficient Mice

scholarly journals TLR2-Dependent Signaling for IL-15 Production Is Essential for the Homeostasis of Intestinal Intraepithelial Lymphocytes

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Yuan Qiu ◽  
Aimin Pu ◽  
Hong Zheng ◽  
Minqiang Liu ◽  
Weigang Chen ◽  
...  
Keyword(s):  
Intestinal Tract ◽  
Dextran Sulfate ◽  
Experimental Colitis ◽  
Intraepithelial Lymphocytes ◽  
Innate Immune ◽  
Intestinal Epithelial ◽  
Rt Pcr ◽  
Intestinal Intraepithelial Lymphocytes ◽  
Deficient Mice ◽  
Tlr2 Signaling

TLR2 signaling is related to colitis and involved in regulation of innate immunity in the intestinal tract, but the mechanisms remain unclear. The aim of this study is to investigate how TLR2 affects differentiation of intraepithelial lymphocytes (IELs) and regulates the susceptibility of colitis. IELs were isolated from the small intestine and colon of mice, respectively. The IEL phenotype, activation, and apoptosis were examined using flow cytometry and RT-PCR. IL-15 expression and IEL location were detected through immunohistochemistry. The experimental colitis was induced by administration of dextran sulfate sodium (DSS). We found that the numbers of CD8αα+, CD8αβ+, and TCRγδ+IELs were significantly decreased in TLR2-deficient mice and the residual IELs displayed reduced activation and proliferation and increased apoptosis, accompanied with impaired IL-15 expression by intestinal epithelial cells (IECs). Further study showed that TLR2 signaling maintained the expression of IL-15 in IEC via NF-κB activation. Moreover, TLR2-deficient mice were found to be more susceptible to DSS-induced colitis as shown by the increased severity of colitis. Our results demonstrate that IECs contribute to the maintenance of IELs at least partly via TLR2-dependent IL-15 production, which provides a clue that may link IECs to innate immune protection of the host via IELs.

c-Myc controls the development of CD8αα TCRαβ intestinal intraepithelial lymphocytes from thymic precursors by regulating IL-15–dependent survival

Blood ◽  
2010 ◽  
Vol 115 (22) ◽  
pp. 4431-4438 ◽  
Author(s):  
Wei Jiang ◽  
Isabel Ferrero ◽  
Elisa Laurenti ◽  
Andreas Trumpp ◽  
H. Robson MacDonald
Keyword(s):  
T Cells ◽  
Large Population ◽  
Cell Receptor ◽  
Intraepithelial Lymphocytes ◽  
Receptor Expression ◽  
Intestinal Intraepithelial Lymphocytes ◽  
Wide Range ◽  
Interleukin 15 ◽  
Secondary Lymphoid Organs ◽  
Deficient Mice

Abstract The murine gut epithelium contains a large population of thymus-derived intraepithelial lymphocytes (IELs), including both conventional CD4+ and CD8αβ+ T cells (expressing T-cell receptor αβ [TCRαβ]) and unconventional CD8αα+ T cells (expressing either TCRαβ or TCRγδ). Whereas conventional IELs are widely accepted to arise from recirculation of activated CD4+ and CD8αβ+ T cells from the secondary lymphoid organs to the gut, the origin and developmental pathway of unconventional CD8αα IELs remain controversial. We show here that CD4-Cre-mediated inactivation of c-Myc, a broadly expressed transcription factor with a wide range of biologic activities, selectively impairs the development of CD8αα TCRαβ IELs. In the absence of c-Myc, CD4− CD8− TCRαβ+ thymic precursors of CD8αα TCRαβ IELs are present but fail to develop on adoptive transfer in immunoincompetent hosts. Residual c-Myc–deficient CD8αα TCRαβ IEL display reduced proliferation and increased apoptosis, which correlate with significantly decreased expression of interleukin-15 receptor subunits and lower levels of the antiapoptotic protein Bcl-2. Transgenic overexpression of human BCL-2 resulted in a pronounced rescue of CD8αα TCRαβ IEL in c-Myc–deficient mice. Taken together, our data support a model in which c-Myc controls the development of CD8αα TCRαβ IELs from thymic precursors by regulating interleukin-15 receptor expression and consequently Bcl-2–dependent survival.

scholarly journals Development of Cd8α/α and Cd8α/β T Cells in Major Histocompatibility Complex Class I–Deficient Mice

1999 ◽  
Vol 190 (6) ◽  
pp. 881-884 ◽  
Author(s):  
Gobardhan Das ◽  
Charles A. Janeway
Keyword(s):  
T Cells ◽  
Major Histocompatibility Complex ◽  
Mhc Class I ◽  
Intraepithelial Lymphocytes ◽  
Class I ◽  
Major Histocompatibility ◽  
Double Knockout ◽  
Intestinal Intraepithelial Lymphocytes ◽  
Histocompatibility Complex ◽  
Deficient Mice

Peripheral CD8+ T cells mainly use CD8α/β, and their development is mainly dependent on the major histocompatibility complex (MHC) class I proteins Kb and Db in H-2b mice. In this report, we have shown that the development of CD8α/β TCR-α/β cells in lymphoid organs as well as in intestinal intraepithelial lymphocytes (iIELs) is dependent on the MHC class I Kb and Db proteins. In contrast, TCR-α/β CD8α/α cells are found mainly in iIELs, and their numbers are unaffected in KbDb double knockout mice. Most of the TCR-γ/δ cells in the iIELs also bear CD8α/α, and they are also unaffected in KbDb −/− mice. In β2-microglobulin (β2m)-deficient mice, all of the TCR-α/β CD8α/α and CD8α/β T cells disappear, but TCR-γ/δ cells are unaffected by the absence of β2m.

scholarly journals Development of Intestinal Intraepithelial Lymphocytes, NK Cells, and NK 1.1+ T Cells in CD45-Deficient Mice

2001 ◽  
Vol 166 (10) ◽  
pp. 6066-6073 ◽  
Author(s):  
Steven M. Martin ◽  
Indira K. Mehta ◽  
Wayne M. Yokoyama ◽  
Matthew L. Thomas ◽  
Robin G. Lorenz
Keyword(s):  
T Cells ◽  
Nk Cells ◽  
Intraepithelial Lymphocytes ◽  
Intestinal Intraepithelial Lymphocytes ◽  
Deficient Mice

scholarly journals CD8α-Deficient Mice Are Highly Susceptible to 5-Fluorouracil-Induced Lethality

2002 ◽  
Vol 9 (3) ◽  
pp. 550-557 ◽  
Author(s):  
Naoto Itoh ◽  
Hitoshi Nishimura ◽  
Tetsuya Matsuguchi ◽  
Toshiki Yajima ◽  
Yasuji Mokuno ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
T Cell ◽  
Homologous Recombination ◽  
T Cell Receptor ◽  
Intestinal Microflora ◽  
Cell Receptor ◽  
Intraepithelial Lymphocytes ◽  
Significant Protection ◽  
Intestinal Intraepithelial Lymphocytes ◽  
Deficient Mice

ABSTRACT Intestinal intraepithelial lymphocytes (i-IEL) expressing CD8α are located in the intestine and may confer protection against invasion of intestinal microflora. We found that mice rendered deficient in CD8α molecules by homologous recombination were susceptible to 5-fluorouracil (5-FU)-induced lethality accompanied by translocation of members of the enterobacteria. The number of i-IEL was greatly reduced on day 6 after 5-FU administration in both CD8α+/− mice and CD8α−/− mice, whereas the recovery of the level of i-IEL thereafter was significantly impaired in CD8α−/− mice compared with that in CD8α+/− mice. The ability of i-IEL to produce gamma interferon in response to immobilized T-cell receptor (TCR) αβ or TCR γδ monoclonal antibodies was significantly lower in CD8α−/− mice than in CD8α+/− mice. Transfer of CD8+ i-IEL conferred significant protection against 5-FU-induced lethality in CD8α−/− mice. The results suggest that CD8+ i-IEL play an important role in protection against 5-FU-induced lethality with translocation of Enterobacteriaceae.

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