Keyword search (4,164 papers available)

"T cell" Keyword-tagged Publications:

Title Authors PubMed ID
1 Nebivolol prevents exhausted T cells and enhances cytotoxicity against MCF-7 breast cancer cells in a β2-adrenergic receptor-dependent manner Hajiaghayi M; Gholizadeh F; Rahbari N; Emamnia N; Shih SCC; Darlington PJ; 41906691
SOH
2 Thermal sonogenetics for adoptive cell transfer therapy Baez A; Hazel K; Guertin Z; Fong E; Manus MM; Kaloyannis A; Helfield B; 41748028
BIOLOGY
3 The age of obesity onset affects changes in subcutaneous adipose tissue macrophages and T cells after weight loss Murphy J; Morais JA; Tsoukas MA; Cooke AB; Daskalopoulou SS; Santosa S; 40831565
SOH
4 Fortifying the Rasamsonia emersonii secretome with recombinant cellobiohydrolase (GH7) for efficient biomass saccharification Raheja Y; Singh V; Gaur VK; Sharma G; Tsang A; Chadha BS; 40622460
GENOMICS
5 The β2-adrenergic receptor agonist terbutaline upregulates T helper-17 cells in a protein kinase A-dependent manner Carvajal Gonczi CM; Hajiaghayi M; Gholizadeh F; Xavier Soares MA; Touma F; Lopez Naranjo C; Rios AJ; Pozzebon C; Daigneault T; Burchell-Reyes K; Darlington PJ; 37438188
PERFORM
6 Loss of function of the carbon catabolite repressor CreA leads to low but inducer-independent expression from the feruloyl esterase B promoter in Aspergillus niger Reijngoud J; Arentshorst M; Ruijmbeek C; Reid I; Alazi ED; Punt PJ; Tsang A; Ram AFJ; 33738610
CSFG
7 Association between rs174537 FADS1 polymorphism and immune cell profiles in abdominal and femoral subcutaneous adipose tissue: an exploratory study in adults with obesity Wang C; Murphy J; Delaney KZ; Khor N; Morais JA; Tsoukas MA; Lowry DE; Mutch DM; Santosa S; 33595419
PERFORM
8 Helper CD4 T cells expressing granzyme B cause glial fibrillary acidic protein fragmentation in astrocytes in an MHCII-independent manner. Stopnicki B, Blain M, Cui QL, Kennedy TE, Antel JP, Healy LM, Darlington PJ 30444064
PERFORM

 

Title:Helper CD4 T cells expressing granzyme B cause glial fibrillary acidic protein fragmentation in astrocytes in an MHCII-independent manner.
Authors:Stopnicki B,  Blain M,  Cui QL,  Kennedy TE,  Antel JP,  Healy LM,  Darlington PJ
Link:https://www.ncbi.nlm.nih.gov/pubmed/30444064?dopt=Abstract
DOI:10.1002/glia.23503
Publication:Glia
Keywords:GFAP;  T cell;  astrocyte;  caspase;  cytoskeleton;  granzyme B;  neuroinflammation; 
PMID:30444064 Category:Glia Date Added:2019-04-15
Dept Affiliation: PERFORM
1 Department of Exercise Science, Department of Biology, PERFORM Centre, Concordia University, Montréal, Quebec, Canada.
2 Department of Neurology and Neurosurgery, Montreal Neurological Institute, and McGill University, Montreal, Quebec, Canada.
3 Neuroimmunology Unit, McGill University, Montréal, Quebec, Canada.

Description:

Helper CD4 T cells expressing granzyme B cause glial fibrillary acidic protein fragmentation in astrocytes in an MHCII-independent manner.

Glia. 2019 04;67(4):582-593

Authors: Stopnicki B, Blain M, Cui QL, Kennedy TE, Antel JP, Healy LM, Darlington PJ

Abstract

During inflammatory processes of the central nervous system, helper T cells have the capacity to cross the blood-brain barrier and injure or kill neural cells through cytotoxic mechanisms. Glial fibrillary acidic protein (GFAP) is an intermediate filament protein that is part of the astrocyte cytoskeleton that can become fragmented in neuroinflammatory conditions. The mechanism of action by which helper T cells with cytotoxic properties injure astrocytes is not completely understood. Primary human astrocytes were obtained from fetal brain tissue. Human helper (CD4+ ) T cells were isolated from peripheral blood mononuclear cells and activated with the superantigen staphylococcal enterotoxin E (SEE). Granzyme B was detected by enzyme linked immunosorbent assay and intracellular flow cytometry. GFAP fragmentation was monitored by western blotting. Cell death was monitored by lactic acid dehydrogenase release and terminal biotin-dUTP nick labeling (TUNEL). Astrocyte migration was monitored by scratch assay. Adult human oligodendrocytes were cultured with sublethally injured astrocytes to determine support function. Helper T cells activated with SEE expressed granzyme B but not perforin. Helper T cells released granzyme B upon contact with astrocytes and caused GFAP fragmentation in a caspase-dependent, MHCII-independent manner. Sublethally injured astrocytes were not apoptotic; however, their processes were thin and elongated, their migration was attenuated, and their ability to support oligodendrocytes was reduced in vitro. Helper T cells can release granzyme B causing sublethal injury to astrocytes, which compromises the supportive functions of astrocytes. Blocking these pathways may lead to improved resolution of neuroinflammatory lesions.

PMID: 30444064 [PubMed - in process]




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