Psychological stress during immunization has minimal effects on the generation and function of CD8+ memory T cells

2006 ◽  
Vol 20 (3) ◽  
pp. 32-33
Author(s):  
John Hunzeker ◽  
Robert H. Bonneau
Keyword(s):  
T Cells ◽  
Psychological Stress ◽  
Memory T Cells ◽  
And Function ◽  
Cd8 Memory T Cells

Controlling the Generation and Function of Human CD8+ Memory T Cells In Vitro with Immunosuppressants

2006 ◽  
Vol 82 (10) ◽  
pp. 1352-1361 ◽  
Author(s):  
Daniel L. Jones ◽  
Steven H. Sacks ◽  
Wilson Wong
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
And Function ◽  
Cd8 Memory T Cells

scholarly journals CD8+Memory T Cells Appear Exhausted within Hours of Acute Virus Infection

2013 ◽  
Vol 191 (8) ◽  
pp. 4211-4222 ◽  
Author(s):  
Martin P. Hosking ◽  
Claudia T. Flynn ◽  
Jason Botten ◽  
J. Lindsay Whitton
Keyword(s):  
T Cells ◽  
Virus Infection ◽  
Memory T Cells ◽  
Cd8 Memory T Cells

CD8 Clonal Expansions in Mice: An Age-associated Alteration of CD8 Memory T-cells

2009 ◽  
pp. 291-325
Author(s):  
Eric T. Clambey ◽  
John W. Kappler ◽  
Philippa Marrack
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
Cd8 Memory T Cells

scholarly journals Impaired Recall of CD8 Memory T Cells in Immunologically Privileged Tissue

2005 ◽  
Vol 174 (3) ◽  
pp. 1165-1170 ◽  
Author(s):  
Zhenhua Dai ◽  
Isam W. Nasr ◽  
Michael Reel ◽  
Songyan Deng ◽  
Lonnette Diggs ◽  
...  
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
Cd8 Memory T Cells

scholarly journals Pulmonary antigen encounter regulates the establishment of tissue-resident CD8 memory T cells in the lung airways and parenchyma

2018 ◽  
Vol 11 (4) ◽  
pp. 1071-1078 ◽  
Author(s):  
Sean R. McMaster ◽  
Alexander N. Wein ◽  
Paul R. Dunbar ◽  
Sarah L. Hayward ◽  
Emily K. Cartwright ◽  
...  
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
Cd8 Memory T Cells ◽  
Lung Airways

scholarly journals Lack of Sprouty 1 and 2 enhances survival of effector CD8+ T cells and yields more protective memory cells

2018 ◽  
Vol 115 (38) ◽  
pp. E8939-E8947 ◽  
Author(s):  
Hesham M. Shehata ◽  
Shahzada Khan ◽  
Elise Chen ◽  
Patrick E. Fields ◽  
Richard A. Flavell ◽  
...  
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
Therapeutic Potential ◽  
Autoimmune Diabetes ◽  
Memory Cells ◽  
Double Knockout ◽  
And Function ◽  
I Cells ◽  
Better Than

Identifying novel pathways that promote robust function and longevity of cytotoxic T cells has promising potential for immunotherapeutic strategies to combat cancer and chronic infections. We show that sprouty 1 and 2 (Spry1/2) molecules regulate the survival and function of memory CD8+ T cells. Spry1/2 double-knockout (DKO) ovalbumin (OVA)-specific CD8+ T cells (OT-I cells) mounted more vigorous autoimmune diabetes than WT OT-I cells when transferred to mice expressing OVA in their pancreatic β-islets. To determine the consequence of Spry1/2 deletion on effector and memory CD8+ T cell development and function, we used systemic infection with lymphocytic choriomeningitis virus (LCMV) Armstrong. Spry1/2 DKO LCMV gp33-specific P14 CD8+ T cells survive contraction better than WT cells and generate significantly more polyfunctional memory T cells. The larger number of Spry1/2 DKO memory T cells displayed enhanced infiltration into infected tissue, demonstrating that absence of Spry1/2 can result in increased recall capacity. Upon adoptive transfer into naive hosts, Spry1/2 DKO memory T cells controlled Listeria monocytogenes infection better than WT cells. The enhanced formation of more functional Spry1/2 DKO memory T cells was associated with significantly reduced mTORC1 activity and glucose uptake. Reduced p-AKT, p-FoxO1/3a, and T-bet expression was also consistent with enhanced survival and memory accrual. Collectively, loss of Spry1/2 enhances the survival of effector CD8+ T cells and results in the formation of more protective memory cells. Deleting Spry1/2 in antigen-specific CD8+ T cells may have therapeutic potential for enhancing the survival and functionality of effector and memory CD8+ T cells in vivo.

scholarly journals Metabolic reprogramming of human CD8+ memory T cells through loss of SIRT1

2017 ◽  
Vol 215 (1) ◽  
pp. 51-62 ◽  
Author(s):  
Mark Y. Jeng ◽  
Philip A. Hull ◽  
Mingjian Fei ◽  
Hye-Sook Kwon ◽  
Chia-Lin Tsou ◽  
...  
Keyword(s):  
T Cells ◽  
Molecular Mechanisms ◽  
Memory T Cells ◽  
Cell Metabolism ◽  
Global Gene Expression ◽  
Metabolic Reprogramming ◽  
Transcriptional Reprogramming ◽  
Age Related ◽  
Global Gene Expression Profiling ◽  
And Function

The expansion of CD8+CD28– T cells, a population of terminally differentiated memory T cells, is one of the most consistent immunological changes in humans during aging. CD8+CD28– T cells are highly cytotoxic, and their frequency is linked to many age-related diseases. As they do not accumulate in mice, many of the molecular mechanisms regulating their fate and function remain unclear. In this paper, we find that human CD8+CD28– T cells, under resting conditions, have an enhanced capacity to use glycolysis, a function linked to decreased expression of the NAD+-dependent protein deacetylase SIRT1. Global gene expression profiling identified the transcription factor FoxO1 as a SIRT1 target involved in transcriptional reprogramming of CD8+CD28– T cells. FoxO1 is proteasomally degraded in SIRT1-deficient CD8+CD28– T cells, and inhibiting its activity in resting CD8+CD28+ T cells enhanced glycolytic capacity and granzyme B production as in CD8+CD28– T cells. These data identify the evolutionarily conserved SIRT1–FoxO1 axis as a regulator of resting CD8+ memory T cell metabolism and activity in humans.

scholarly journals CD40L expression permits CD8+ T cells to execute immunologic helper functions

Blood ◽  
2013 ◽  
Vol 122 (3) ◽  
pp. 405-412 ◽  
Author(s):  
Marco Frentsch ◽  
Regina Stark ◽  
Nadine Matzmohr ◽  
Sarah Meier ◽  
Sibel Durlanik ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd8 T Cells ◽  
Major Part ◽  
Memory T Cells ◽  
Helper T Cells ◽  
Key Points ◽  
Cd40l Expression ◽  
Cd8 Memory T Cells

Key Points A major part of CD8+ memory T cells expresses CD40L, the key molecule for T-cell–dependent help. CD40L-expressing CD8+ T cells resemble functional CD4+ helper T cells.

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