T-cell-specific deletion of gp130 renders the highly susceptible IL-10-deficient mouse resistant to intestinal nematode infection

2009 ◽  
Vol 39 (8) ◽  
pp. 2173-2183 ◽  
Author(s):  
Nicolas Fasnacht ◽  
Marina C. Greweling ◽  
Mariela Bollati-Fogolín ◽  
Angela Schippers ◽  
Werner Müller
Keyword(s):  
T Cell ◽  
Nematode Infection ◽  
Deficient Mouse ◽  
Intestinal Nematode ◽  
Specific Deletion

scholarly journals PD-L1 – PD-1 interactions limit effector Treg cell populations at homeostasis and during infection

2020 ◽  
Author(s):  
J.A. Perry ◽  
J.T. Clark ◽  
J. Gullicksrud ◽  
J. DeLong ◽  
L. Shallberg ◽  
...  
Keyword(s):  
T Cell ◽  
Treg Cell ◽  
Cell Activity ◽  
T Cell Responses ◽  
Treg Cells ◽  
Whole Body ◽  
Cell Responses ◽  
Early Production ◽  
Ifn Γ ◽  
Specific Deletion

AbstractWhile much is known about the factors that promote the development of diverse Treg cell responses, less is known about the pathways that constrain Treg cell activities. The studies presented here reveal that at homeostasis there is a population of effector Treg cells that express PD-1, and that blockade of PD-L1 or loss of PD-1 results in increased Treg cell activity. In response to infection with the parasite T. gondii, the early production of IFN-γ results in widespread upregulation of PD-L1. Moreover, blockade of PD-L1, whole body deletion of PD-1, or lineage-specific deletion of PD-1 in Foxp3+ cells prevented the loss of the effector Treg cells but resulted in reduced pathogen specific CD4+ T cell responses during infection. Thus, at homeostasis basal PD-L1 expression constrains and tunes the pool of Treg cells, but during infection the upregulation of PD-L1 provides a mechanism to contract the Treg cell population required to maximize the development of pathogen specific CD4+ T cell responses.

The CD4 T cell-deficient mouse mutation nackt ( nkt ) involves a deletion in the cathepsin L ( Ctsl ) gene

2001 ◽  
Vol 53 (3) ◽  
pp. 233-242 ◽  
Author(s):  
Fernando Benavides ◽  
Ann Venables ◽  
Heather Poetschke Klug ◽  
Edward Glasscock ◽  
Natalia Martin Palenzuela ◽  
...  
Keyword(s):  
T Cell ◽  
Cathepsin L ◽  
Cd4 T Cell ◽  
Deficient Mouse ◽  
Mouse Mutation

scholarly journals T cell-intrinsic role of IL-6 signaling in primary and memory responses

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Simone A Nish ◽  
Dominik Schenten ◽  
F Thomas Wunderlich ◽  
Scott D Pope ◽  
Yan Gao ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Suppressive Effect ◽  
Immune Recognition ◽  
Th17 Response ◽  
Cell Responses ◽  
Underlying Mechanisms ◽  
Specific Deletion

Innate immune recognition is critical for the induction of adaptive immune responses; however the underlying mechanisms remain incompletely understood. In this study, we demonstrate that T cell-specific deletion of the IL-6 receptor α chain (IL-6Rα) results in impaired Th1 and Th17 T cell responses in vivo, and a defect in Tfh function. Depletion of Tregs in these mice rescued the Th1 but not the Th17 response. Our data suggest that IL-6 signaling in effector T cells is required to overcome Treg-mediated suppression in vivo. We show that IL-6 cooperates with IL-1β to block the suppressive effect of Tregs on CD4+ T cells, at least in part by controlling their responsiveness to IL-2. In addition, although IL-6Rα-deficient T cells mount normal primary Th1 responses in the absence of Tregs, they fail to mature into functional memory cells, demonstrating a key role for IL-6 in CD4+ T cell memory formation.

scholarly journals T-cell-specific deletion of Mof blocks their differentiation and results in genomic instability in mice

Mutagenesis ◽  
2013 ◽  
Vol 28 (3) ◽  
pp. 263-270 ◽  
Author(s):  
Arun Gupta ◽  
Clayton R. Hunt ◽  
Raj K. Pandita ◽  
Juhee Pae ◽  
K. Komal ◽  
...  
Keyword(s):  
T Cell ◽  
Genomic Instability ◽  
Specific Deletion

scholarly journals The RNAseIII enzyme Drosha is critical in T cells for preventing lethal inflammatory disease

2008 ◽  
Vol 205 (9) ◽  
pp. 2005-2017 ◽  
Author(s):  
Mark M.W. Chong ◽  
Jeffrey P. Rasmussen ◽  
Alexander Y. Rudensky ◽  
Dan R. Littman
Keyword(s):  
T Cell ◽  
Inflammatory Disease ◽  
Cell Types ◽  
Mirna Biogenesis ◽  
Cell Compartment ◽  
Foxp3 Gene ◽  
Genetic Ablation ◽  
And Function ◽  
Specific Deletion

MicroRNAs (miRNAs) are implicated in the differentiation and function of many cell types. We provide genetic and in vivo evidence that the two RNaseIII enzymes, Drosha and Dicer, do indeed function in the same pathway. These have previously been shown to mediate the stepwise maturation of miRNAs (Lee, Y., C. Ahn, J. Han, H. Choi, J. Kim, J. Yim, J. Lee, P. Provost, O. Radmark, S. Kim, and V.N. Kim. 2003. Nature. 425:415–419), and genetic ablation of either within the T cell compartment, or specifically within Foxp3+ regulatory T (T reg) cells, results in identical phenotypes. We found that miRNA biogenesis is indispensable for the function of T reg cells. Specific deletion of either Drosha or Dicer phenocopies mice lacking a functional Foxp3 gene or Foxp3+ cells, whereas deletion throughout the T cell compartment also results in spontaneous inflammatory disease, but later in life. Thus, miRNA-dependent regulation is critical for preventing spontaneous inflammation and autoimmunity.

scholarly journals Intestinal Nematode Infection Ameliorates Experimental Colitis in Mice

2002 ◽  
Vol 70 (11) ◽  
pp. 5931-5937 ◽  
Author(s):  
W. I. Khan ◽  
P. A. Blennerhasset ◽  
A. K. Varghese ◽  
S. K. Chowdhury ◽  
P. Omsted ◽  
...  
Keyword(s):  
Immune Response ◽  
Trichinella Spiralis ◽  
Experimental Colitis ◽  
Developed Countries ◽  
Epidemiological Studies ◽  
Nematode Infection ◽  
Th2 Cells ◽  
Th2 Response ◽  
Th1 Cell ◽  
Intestinal Nematode

ABSTRACT Epidemiological studies suggest that inflammatory bowel disease (IBD) is common in developed countries and rare in countries where intestinal nematode infections are common. T cells are critical in many immune responses, including those associated with IBD and nematode infection. Among the distinct T helper (Th) cell subsets, Th1-type immune response is predominantly associated with Crohn's disease, while many nematode infections generate a strong Th2 response. The reciprocal cross regulation between Th1 and Th2 cells suggests that generation of a Th2 response by nematodes could prevent or reduce the effects of Th1-mediated diseases. In the present study, we investigated the effect of polarizing the immune response toward the Th2 type, using intestinal nematode infection, on subsequent experimental colitis. Mice were infected with the intestinal nematode Trichinella spiralis and allowed to recover before colitis was induced with dinitrobenzene sulfonic acid. The mice were sacrificed postcolitis to assess colonic damage macroscopically, histologically, and by myeloperoxidase (MPO) activity and Th cytokines. Prior nematode infection reduced the severity of colitis both macroscopically and histologically together with a decreased mortality and was correlated with a down-regulation of MPO activity, Th1-type cytokine expression in colonic tissue, and emergence of a Th2-type immune response. These results indicate a protective role of nematode infection in Th1 cell-driven inflammation and prompt consideration of a novel therapeutic strategy in IBD based on immunological distraction.

scholarly journals Interplay between Th1 and Th17 effector T-cell pathways in the pathogenesis of spontaneous colitis and colon cancer in the G i2-deficient mouse

2012 ◽  
Vol 25 (1) ◽  
pp. 35-44 ◽  
Author(s):  
Y.-Y. Gotlind ◽  
M. Fritsch Fredin ◽  
A. K. Kumawat ◽  
H. Strid ◽  
R. Willen ◽  
...  
Keyword(s):  
Colon Cancer ◽  
T Cell ◽  
Deficient Mouse ◽  
Effector T Cell
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