Polyclonal expansion of adoptively transferred CD4+ αβ T cells in the colonic lamina propria of scid mice with colitis

1996 ◽  
Vol 26 (5) ◽  
pp. 1156-1163 ◽  
Author(s):  
Angelika Rudolphi ◽  
Kerstin Bonhagen ◽  
Jörg Reimann
Keyword(s):  
T Cells ◽  
Lamina Propria ◽  
Scid Mice ◽  
Αβ T Cells

Cytotoxic reactivity of gut lamina propria CD4+ αβ T cells in SCID mice with colitis

1996 ◽  
Vol 26 (12) ◽  
pp. 3074-3083 ◽  
Author(s):  
Kerstin Bonhagen ◽  
Stefan Thoma ◽  
Paul Bland ◽  
Søren Bregenholt ◽  
Angelika Rudolphi ◽  
...  
Keyword(s):  
T Cells ◽  
Lamina Propria ◽  
Scid Mice ◽  
Αβ T Cells

The majority of lamina propria CD4+ T-cells from scid mice with colitis undergo Fas-mediated apoptosis in vivo

2001 ◽  
Vol 78 (1) ◽  
pp. 7-12 ◽  
Author(s):  
Søren Bregenholt ◽  
Troels R. Petersen ◽  
Mogens H. Claesson
Keyword(s):  
T Cells ◽  
Lamina Propria ◽  
Cd4 T Cells ◽  
Scid Mice

scholarly journals The Microbiota Contributes to CD8+T Cell Activation and Nutrient Malabsorption following Intestinal Infection with Giardia duodenalis

2016 ◽  
Vol 84 (10) ◽  
pp. 2853-2860 ◽  
Author(s):  
Aleksander Keselman ◽  
Erqiu Li ◽  
Jenny Maloney ◽  
Steven M. Singer
Keyword(s):  
T Cells ◽  
T Cell ◽  
Immune Responses ◽  
Lamina Propria ◽  
Antibiotic Treatment ◽  
T Cell Activation ◽  
Cell Activation ◽  
Giardia Duodenalis ◽  
Content Type ◽  
Αβ T Cells

Giardia duodenalisis a noninvasive luminal pathogen that impairs digestive function in its host in part by reducing intestinal disaccharidase activity. This enzyme deficiency has been shown in mice to require CD8+T cells. We recently showed that both host immune responses and parasite strain affected disaccharidase levels during murine giardiasis. However, high doses of antibiotics were used to facilitate infections in that study, and we therefore decided to systematically examine the effects of antibiotic use on pathogenesis and immune responses in the mouse model of giardiasis. We found that antibiotic treatment did not overtly increase the parasite burden but significantly limited the disaccharidase deficiency observed in infected mice. Moreover, while infected mice had more activated CD8+αβ T cells in the small intestinal lamina propria, this increase was absent in antibiotic-treated mice. Infection also led to increased numbers of CD4+αβ T cells in the lamina propria and activation of T cell receptor γδ-expressing intraepithelial lymphocytes (IEL), but these changes were not affected by antibiotics. Finally, we show that activated CD8+T cells express gamma interferon (IFN-γ) and granzymes but that granzymes are not required for sucrase deficiency. We conclude that CD8+T cells become activated in giardiasis through an antibiotic-sensitive process and contribute to reduced sucrase activity. These are the first data directly demonstrating activation of CD8+T cells and γδ T cells duringGiardiainfections. These data also demonstrate that disruption of the intestinal microbiota by antibiotic treatment prevents pathological CD8+T cell activation in giardiasis.

Blockade of NKG2D signaling prevents the development of murine CD4+ T cell-mediated colitis

2008 ◽  
Vol 294 (1) ◽  
pp. G199-G207 ◽  
Author(s):  
Y. Ito ◽  
T. Kanai ◽  
T. Totsuka ◽  
R. Okamoto ◽  
K. Tsuchiya ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Natural Killer ◽  
Lamina Propria ◽  
Intestinal Inflammation ◽  
Constitutive Expression ◽  
Γδ T Cells ◽  
Scid Mice ◽  
Costimulatory Receptor ◽  
Bowel Diseases

It has been recently demonstrated that NKG2D is an activating costimulatory receptor on natural killer (NK) cells, natural killer T (NKT) cells, activated CD8+ T cells, and γδ T cells, which respond to cellular stress, such as inflammation, transformation, and infection. Here we show that intestinal inflammation in colitic SCID mice induced by adoptive transfer of CD4+CD45RBhigh T cells is characterized by significant increase of CD4+NKG2D+ T cells and constitutive expression of NKG2D ligands, such as H60, Mult-1, and Rae-1, by lamina propria CD11c+ dendritic cells. Furthermore, treatment with nondepleting and neutralizing anti-NKG2D MAb after transfer of CD4+CD45RBhigh T cells into SCID mice significantly suppressed wasting disease with colitis, abrogated leukocyte infiltration, and reduced production of IFN-γ by lamina propria CD4+ T cells. These findings demonstrate that NKG2D signaling pathway is critically involved in CD4+ T cell-mediated disease progression and suggest a new therapeutic target for inflammatory bowel diseases.

scholarly journals CD40/CD40L contributes to hypercholesterolemia-induced microvascular inflammation

2009 ◽  
Vol 296 (3) ◽  
pp. H689-H697 ◽  
Author(s):  
Karen Y. Stokes ◽  
LeShanna Calahan ◽  
Candiss M. Hamric ◽  
Janice M. Russell ◽  
D. Neil Granger
Keyword(s):  
Oxidative Stress ◽  
T Cells ◽  
T Cell ◽  
Blood Cell ◽  
Cell Function ◽  
Inflammatory Responses ◽  
Microvascular Dysfunction ◽  
Cd40 Ligand ◽  
Scid Mice ◽  
Endothelial Cell Function

Hypercholesterolemia is associated with phenotypic changes in endothelial cell function that lead to a proinflammatory and prothrombogenic state in different segments of the microvasculature. CD40 ligand (CD40L) and its receptor CD40 are ubiquitously expressed and mediate inflammatory responses and platelet activation. The objective of this study was to determine whether CD40/CD40L, in particular T-cell CD40L, contributes to microvascular dysfunction induced by hypercholesterolemia. Intravital microscopy was used to quantify blood cell adhesion in cremasteric postcapillary venules, endothelium-dependent vasodilation responses in arterioles, and microvascular oxidative stress in wild-type (WT) C57BL/6, CD40-deficient (−/−), CD40L−/−, or severe combined immune deficient (SCID) mice placed on a normal (ND) or high-cholesterol (HC) diet for 2 wk. WT-HC mice exhibited an exaggerated leukocyte and platelet recruitment in venules and impaired vasodilation responses in arterioles compared with ND counterparts. A deficiency of CD40, CD40L, or lymphocytes attenuated these responses to HC. The HC phenotype was rescued in CD40L−/− and SCID mice by a transfer of WT T cells. Bone marrow chimeras revealed roles for both vascular- and blood cell-derived CD40 and CD40L in the HC-induced vascular responses. Hypercholesterolemia induced an oxidative stress in both arterioles and venules of WT mice, which was abrogated by either CD40 or CD40L deficiency. The transfer of WT T cells into CD40L−/− mice restored the oxidative stress. These results implicate CD40/CD40L interactions between circulating cells and the vascular wall in both the arteriolar and venular dysfunction elicited by hypercholesterolemia and identify T-cell-associated CD40L as a key mediator of these responses.

scholarly journals In vitro co-culture of human intestinal organoids and lamina propria-derived CD4+ T cells

2021 ◽  
Vol 2 (2) ◽  
pp. 100519
Author(s):  
Renée R.C.E. Schreurs ◽  
Martin E. Baumdick ◽  
Agata Drewniak ◽  
Madeleine J. Bunders
Keyword(s):  
T Cells ◽  
Lamina Propria ◽  
Cd4 T Cells ◽  
Intestinal Organoids
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