T‐Cell Differentiation to T Helper 9 Phenotype is Elevated by Extremely Low‐Frequency Electromagnetic Fields Via Induction of IL‐2 Signaling

2019 ◽  
Vol 40 (8) ◽  
pp. 588-601
Author(s):  
Ye Won Jang ◽  
Ki Cheol Gil ◽  
Ji Soo Lee ◽  
WonKu Kang ◽  
So‐Young Park ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
T Cell ◽  
Electromagnetic Fields ◽  
Low Frequency ◽  
T Cell Differentiation ◽  
T Helper ◽  
Extremely Low Frequency

scholarly journals Potential Antiinflammatory Role of Insulin via the Preferential Polarization of Effector T Cells toward a T Helper 2 Phenotype

Endocrinology ◽  
2007 ◽  
Vol 148 (1) ◽  
pp. 346-353 ◽  
Author(s):  
Alexander Viardot ◽  
Shane T. Grey ◽  
Fabienne Mackay ◽  
Donald Chisholm
Keyword(s):  
T Cells ◽  
Cell Differentiation ◽  
T Cell ◽  
Insulin Receptor ◽  
T Cell Differentiation ◽  
Receptor Expression ◽  
T Helper ◽  
Type Response ◽  
Helper Type

Hyperglycemia in critical illness is a common complication and a strong independent risk factor for morbidity and death. Intensive insulin therapy decreases this risk by up to 50%. It is unclear to what extent this benefit is due to reversal of glucotoxicity or to a direct effect of insulin, because antiinflammatory effects of insulin have already been described, but the underlying mechanisms are still poorly understood. The insulin receptor is expressed on resting neutrophils, monocytes, and B cells, but is not detectable on T cells. However, significant up-regulation of insulin receptor expression is observed on activated T cells, which suggests an important role during T cell activation. Exogenous insulin in vitro induced a shift in T cell differentiation toward a T helper type 2 (Th2)-type response, decreasing the T helper type 1 to Th2 ratio by 36%. This result correlated with a corresponding change in cytokine secretion, with the interferon-γ to IL-4 ratio being decreased by 33%. These changes were associated with increased Th2-promoting ERK phosphorylation in the presence of insulin. Thus, we demonstrate for the first time that insulin treatment influences T cell differentiation promoting a shift toward a Th2-type response. This effect of insulin in changing T cell polarization may contribute to its antiinflammatory role not only in sepsis, but also in chronic inflammation associated with obesity and type 2 diabetes.

Micro-RNA Profiling in CD4+ T Cell Differentiation.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3887-3887
Author(s):  
Arnob Banerjee ◽  
Felix Schambach ◽  
Scott Hammond ◽  
Steven Reiner
Keyword(s):  
T Cells ◽  
Cell Differentiation ◽  
T Cell ◽  
Cd4 T Cells ◽  
Expression Profiles ◽  
T Cell Differentiation ◽  
Micro Rna ◽  
Cd4 T Cell ◽  
T Helper ◽  
Micro Rnas

Abstract Micro-RNAs comprise a class of small noncoding RNAs which have been found to be important regulators of cellular differentiation in multiple species. Previous analysis of micro-RNA expression in the murine hematopoietic system has suggested a role in cell differentiation and the maintenance of cell identity. Naïve progenitor CD4+ T cells respond to a combination of appropriate antigen and other specific signals by undergoing proliferation and further differentiation into one of at least two subsets. T helper 1 (TH1) cells produce high levels of the cytokine IFN-γ and T helper 2 (TH2) cells produce high levels of IL-4, optimizing them for control of intracellular and extracellular pathogens, respectively. It is currently not known whether micro-RNA molecules influence CD4+ T cell differentiation. We have used oligonucleotide arrays to analyze micro-RNA expression profiles of freshly isolated murine CD4+ T cells compared to cells differentiating into TH1 and TH2 subsets. Expression profiles were found to differ significantly between naïve and stimulated CD4+ cells, with fewer differences between TH1 and TH2 subsets. Promising candidate micro-RNAs are being further evaluated by northern blot and genetic studies. Micro-RNA-155 is upregulated on stimulation of CD4+ T cells in multiple oligonucleotide array assays. Micro-RNA-155 is encoded by the BIC oncogene and has been implicated in lymphomagenesis as well as in other malignancies. We have verified the induction of micro-RNA-155 in stimulated helper T cells by northern blot and are studying the effects of this micro-RNA on CD4+ T cell differentiation. Our observations support a role for micro-RNAs in helper T cell differentiation during the immune response.

scholarly journals STAT3 signaling in myeloid cells promotes pathogenic myelin-specific T cell differentiation and autoimmune demyelination

2020 ◽  
Vol 117 (10) ◽  
pp. 5430-5441 ◽  
Author(s):  
Hsueh Chung Lu ◽  
Sunja Kim ◽  
Andrew J. Steelman ◽  
Kevin Tracy ◽  
Beiyan Zhou ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
T Cell ◽  
Demyelinating Disease ◽  
Myeloid Cells ◽  
Myeloid Cell ◽  
T Cell Differentiation ◽  
Mutant Mice ◽  
T Helper ◽  
Myeloid Lineage ◽  
Stat3 Signaling

Multiple sclerosis (MS) is an autoimmune inflammatory demyelinating disease of the central nervous system. Dysregulation of STAT3, a transcription factor pivotal to various cellular processes including Th17 cell differentiation, has been implicated in MS. Here, we report that STAT3 is activated in infiltrating monocytic cells near active MS lesions and that activation of STAT3 in myeloid cells is essential for leukocyte infiltration, neuroinflammation, and demyelination in experimental autoimmune encephalomyelitis (EAE). Genetic disruption of Stat3 in peripheral myeloid lineage cells abrogated EAE, which was associated with decreased antigen-specific T helper cell responses. Myeloid cells from immunized Stat3 mutant mice exhibited impaired antigen-presenting functions and were ineffective in driving encephalitogenic T cell differentiation. Single-cell transcriptome analyses of myeloid lineage cells from preclinical wild-type and mutant mice revealed that loss of myeloid STAT3 signaling disrupted antigen-dependent cross-activation of myeloid cells and T helper cells. This study identifies a previously unrecognized requisite for myeloid cell STAT3 in the activation of myelin-reactive T cells and suggests myeloid STAT3 as a potential therapeutic target for autoimmune demyelinating disease.

scholarly journals Oxidative Stress Promotes Polarization of Human T Cell Differentiation Toward a T Helper 2 Phenotype

2006 ◽  
Vol 176 (5) ◽  
pp. 2765-2772 ◽  
Author(s):  
Miranda R. King ◽  
Anisa S. Ismail ◽  
Laurie S. Davis ◽  
David R. Karp
Keyword(s):  
Oxidative Stress ◽  
Cell Differentiation ◽  
T Cell ◽  
T Cell Differentiation ◽  
T Helper ◽  
T Helper 2 ◽  
Human T Cell

scholarly journals New Insights into Epigenetic Regulation of T Cell Differentiation

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3459
Author(s):  
Avik Dutta ◽  
Harini Venkataganesh ◽  
Paul E. Love
Keyword(s):  
Dna Methylation ◽  
T Cells ◽  
Cell Differentiation ◽  
T Cell ◽  
Epigenetic Regulation ◽  
Cd8 T Cells ◽  
Cytotoxic T Cells ◽  
T Cell Differentiation ◽  
T Helper ◽  
Epigenetic Regulators

Immature CD4− CD8− thymocytes progress through several developmental steps in the thymus, ultimately emerging as mature CD4+ (helper) or CD8+ (cytotoxic) T cells. Activation of naïve CD4+ and CD8+ T cells in the presence of specific cytokines results in the induction of transcriptional programs that result in their differentiation into effector or memory cells and in the case of CD4+ T cells, the adoption of distinct T-helper fates. Previous studies have shown that histone modification and DNA methylation play important roles in each of these events. More recently, the roles of specific epigenetic regulators in T cell differentiation have been clarified. The identification of the epigenetic modifications and modifiers that control mature T cell differentiation and specification has also provided further insights into how dysregulation of these processes can lead to cancer or autoimmune diseases. In this review, we summarize recent findings that have provided new insights into epigenetic regulation of T cell differentiation in both mice and humans.

scholarly journals Characterization of T Cell Differentiation in the Murine Gut

2002 ◽  
Vol 195 (4) ◽  
pp. 437-449 ◽  
Author(s):  
Florence Lambolez ◽  
Orly Azogui ◽  
Anne-Marie Joret ◽  
Corinne Garcia ◽  
Harald von Boehmer ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
T Cell ◽  
Mrna Expression ◽  
Low Frequency ◽  
T Cell Differentiation ◽  
Recombination Activating Gene ◽  
Local Differentiation ◽  
Rag 1 ◽  
The Impact ◽  
Kinetics Of

Gut intraepithelial CD8 T lymphocytes (T-IEL) are distinct from thymus-derived cells and are thought to derive locally from cryptopatch (CP) precursors. The intermediate stages of differentiation between CP and mature T-IEL were not identified, and the local differentiation process was not characterized. We identified and characterized six phenotypically distinct lineage-negative populations in the CP and the gut epithelium: (a) we determined the kinetics of their generation from bone marrow precursors; (b) we quantified CD3-ϵ, recombination activating gene (Rag)-1, and pre-Tα mRNAs expression at single cell level; (c) we characterized TCR-β, -γ, and -α locus rearrangements; and (d) we studied the impact of different mutations on the local differentiation. These data allowed us to establish a sequence of T cell precursor differentiation in the gut. We also observed that the gut differentiation varied from that of the thymus by a very low frequency of pre-Tα chain mRNA expression, a different kinetics of Rag-1 mRNA expression, and a much higher impact of CD3 ϵ/δ and pre-Tα deficiencies. Finally, only 3% of CP cells were clearly involved in T cell differentiation, suggesting that these structures may have additional physiological roles in the gut.

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