Phenotype and function of circulating memory T cells in human vitiligo*

2020 ◽  
Vol 183 (5) ◽  
pp. 899-908 ◽  
Author(s):  
C. Martins ◽  
A.‐S. Darrigade ◽  
C. Jacquemin ◽  
T. Barnetche ◽  
A. Taieb ◽  
...  
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
And Function

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 In Vivo Blockade of Murine ARTC2.2 During Cell Preparation Preserves the Vitality and Function of Liver Tissue-Resident Memory T Cells

2018 ◽  
Vol 9 ◽  
Author(s):  
Björn Rissiek ◽  
Marco Lukowiak ◽  
Friederike Raczkowski ◽  
Tim Magnus ◽  
Hans-Willi Mittrücker ◽  
...  
Keyword(s):  
T Cells ◽  
Liver Tissue ◽  
Memory T Cells ◽  
Cell Preparation ◽  
And Function ◽  
Resident Memory T Cells

scholarly journals Immune Dysregulation after Cardiothoracic Surgery and Incidental Thymectomy: Maintenance of Regulatory T Cells despite Impaired Thymopoiesis

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Nancy J. Halnon ◽  
Paige Cooper ◽  
Diana Yu Hui Chen ◽  
M. Ines Boechat ◽  
Christel H. Uittenbogaart
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Congenital Heart ◽  
Memory T Cells ◽  
Immune Dysregulation ◽  
Cardiothoracic Surgery ◽  
Immune Disorders ◽  
Treg Number ◽  
And Function ◽  
Dsdna Antibodies

Thymectomy is performed in infants during cardiothoracic surgery leaving many patients with reduced thympopoiesis. An association between immune disorders and regulatory T cells (Treg) after incidental thymectomy has not been investigated. Questionnaires soliciting symptoms of atopic or autoimmune disease and biomarkers were measured in children and adults with congenital heart disease and either reduced or preserved thymopoiesis. Tregs were examined. Atopic or autoimmune-like symptoms and elevated anti-dsDNA antibodies were common after surgery in individuals with low thymopoiesis. Total Treg number and function were maintained but with fewer naïve Treg. TCR spectratypes were similar to other memory T cells. These data suggest that thymectomy does not reduce total Treg number but homeostasis is affected with reduced naïve Treg. Prevalence of autoimmune or atopic symptoms after surgery is not associated with total number or proportion of Tregs but appears to be due to otherwise unknown factors that may include altered Treg homeostasis.

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

Fate and function of anti-CD3/CD28-activated T cells following adoptive transfer: IL-2 promotes development of anti-tumor memory T cells in vivo

Cytotherapy ◽  
2005 ◽  
Vol 7 (5) ◽  
pp. 396-407 ◽  
Author(s):  
D.P.M. Hughes ◽  
D. Baskar ◽  
F.A. Urban ◽  
M.S. Friedman ◽  
T.M. Braun ◽  
...  
Keyword(s):  
T Cells ◽  
Adoptive Transfer ◽  
Memory T Cells ◽  
Activated T Cells ◽  
And Function

scholarly journals Progressive change in expression of killer-like receptorsr and GPR56 expression defines the cytokine production potential of human CD4+ T memory cells

2017 ◽  
Author(s):  
Kim-Long Truong ◽  
Stephan Schlickeiser ◽  
Katrin Vogt ◽  
David Boës ◽  
Julia Schumann ◽  
...  
Keyword(s):  
T Cells ◽  
Cytokine Production ◽  
Memory T Cells ◽  
Single Gene ◽  
Effector Memory ◽  
Functional Heterogeneity ◽  
Production Potential ◽  
Progressive Change ◽  
And Function ◽  
Common Understanding

AbstractMemory T cells mount an accelerated response upon re-challenge but are heterogeneous in phenotype and function. Traditionally memory T cells were classified into central memory, effector memory and terminally differentiated effector memory (TEMRA) cells based on expression of CCR7 and CD45RA. Functional heterogeneity even within these subsets demonstrated the need for more suitable markers. We applied bulk and single gene expression profiling of human CD4+ memory T cells and identified surface markers, KLRB1, KLRG1, GPR56 and KLRF1, allowing classification into “low”, “high” or “exhausted” cytokine producers. In contrast to common understanding KLRG1 expression was not associated with exhaustion and highest production of multiple cytokines was observed in KLRB1+KLRG1+GPR56+ T cells. Only additional KLRF1 expression was associated with a decline in cytokine production. The superiority of KLRF1 to define exhausted cytokine producers compared to classical TEMRA identification was best exemplified for intrahepatic T cells in patients with inflammatory liver diseases.

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