scholarly journals Corrigendum to “Erythroid differentiation regulator 1 strengthens TCR signaling in thymocytes by modulating calcium flux” [Cell. Immunol. 336 (2019) 28–33]

2022 ◽  
pp. 104474
Author(s):  
Myun Soo Kim ◽  
Sora Lee ◽  
Su-Jin Jung ◽  
Sunyoung Park ◽  
Kyung Eun Kim ◽  
...  
Keyword(s):  
Erythroid Differentiation ◽  
Calcium Flux ◽  
Tcr Signaling

Erythroid differentiation regulator 1 strengthens TCR signaling in thymocytes by modulating calcium flux

2019 ◽  
Vol 336 ◽  
pp. 28-33 ◽  
Author(s):  
Myun Soo Kim ◽  
Sora Lee ◽  
Su-Jin Jung ◽  
Sunyoung Park ◽  
Kyung Eun Kim ◽  
...  
Keyword(s):  
Erythroid Differentiation ◽  
Calcium Flux ◽  
Tcr Signaling

scholarly journals BCL11B is required for positive selection and survival of double-positive thymocytes

2007 ◽  
Vol 204 (12) ◽  
pp. 3003-3015 ◽  
Author(s):  
Diana I. Albu ◽  
Dongyun Feng ◽  
Debarati Bhattacharya ◽  
Nancy A. Jenkins ◽  
Neal G. Copeland ◽  
...  
Keyword(s):  
Positive Selection ◽  
Transcriptional Control ◽  
Critical Role ◽  
Cell Receptor ◽  
Calcium Flux ◽  
Tcr Signaling ◽  
Double Positive ◽  
Control Of Gene Expression ◽  
Altered Expression ◽  
Selection Of

Transcriptional control of gene expression in double-positive (DP) thymocytes remains poorly understood. We show that the transcription factor BCL11B plays a critical role in DP thymocytes by controlling positive selection of both CD4 and CD8 lineages. BCL11B-deficient DP thymocytes rearrange T cell receptor (TCR) α; however, they display impaired proximal TCR signaling and attenuated extracellular signal-regulated kinase phosphorylation and calcium flux, which are all required for initiation of positive selection. Further, provision of transgenic TCRs did not improve positive selection of BCL11B-deficient DP thymocytes. BCL11B-deficient DP thymocytes have altered expression of genes with a role in positive selection, TCR signaling, and other signaling pathways intersecting the TCR, which may account for the defect. BCL11B-deficient DP thymocytes also presented increased susceptibility to spontaneous apoptosis associated with high levels of cleaved caspase-3 and an altered balance of proapoptotic/prosurvival factors. This latter susceptibility was manifested even in the absence of TCR signaling and was only partially rescued by provision of the BCL2 transgene, indicating that control of DP thymocyte survival by BCL11B is nonredundant and, at least in part, independent of BCL2 prosurvival factors.

scholarly journals Regulation of positive and negative selection and TCR signaling during thymic T cell development by capicua

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Soeun Kim ◽  
Guk-Yeol Park ◽  
Jong Seok Park ◽  
Jiho Park ◽  
Hyebeen Hong ◽  
...  
Keyword(s):  
T Cell ◽  
Negative Selection ◽  
Target Genes ◽  
Selection Process ◽  
T Cell Development ◽  
Cell Development ◽  
Calcium Flux ◽  
Thymic Selection ◽  
Tcr Signaling ◽  
Selection Of

Central tolerance is achieved through positive and negative selection of thymocytes mediated by T cell receptor (TCR) signaling strength. Thus, dysregulation of the thymic selection process often leads to autoimmunity. Here, we show that Capicua (CIC), a transcriptional repressor that suppresses autoimmunity, controls the thymic selection process. Loss of CIC prior to T-cell lineage commitment impairs both positive and negative selection of thymocytes. CIC deficiency attenuated TCR signaling in CD4+CD8+ double-positive (DP) cells, as evidenced by a decrease in CD5 and phospho-ERK levels and calcium flux. We identified Spry4, Dusp4, Dusp6, and Spred1 as CIC target genes that could inhibit TCR signaling in DP cells. Furthermore, impaired positive selection and TCR signaling were partially rescued in Cic and Spry4 double mutant mice. Our findings indicate that CIC is a transcription factor required for thymic T cell development and suggests that CIC acts at multiple stages of T cell development and differentiation to prevent autoimmunity.

scholarly journals Erythroid Differentiation Regulator 1 Strengthens TCR Signaling by Enhancing PLCγ1 Signal Transduction Pathway

2022 ◽  
Vol 23 (2) ◽  
pp. 844
Author(s):  
Myun Soo Kim ◽  
Dongmin Park ◽  
Sora Lee ◽  
Sunyoung Park ◽  
Kyung Eun Kim ◽  
...  
Keyword(s):  
Signal Transduction ◽  
T Cells ◽  
Cd4 T Cells ◽  
Signal Transduction Pathway ◽  
Erythroid Differentiation ◽  
Transduction Pathway ◽  
Tcr Signaling ◽  
Peripheral T Cells ◽  
Signal Regulation

Erythroid differentiation regulator 1 (Erdr1) has previously been reported to control thymocyte selection via TCR signal regulation, but the effect of Erdr1 as a TCR signaling modulator was not studied in peripheral T cells. In this report, it was determined whether Erdr1 affected TCR signaling strength in CD4 T cells. Results revealed that Erdr1 significantly enhanced the anti-TCR antibody-mediated activation and proliferation of T cells while failing to activate T cells in the absence of TCR stimulation. In addition, Erdr1 amplified Ca2+ influx and the phosphorylation of PLCγ1 in CD4 T cells with the TCR stimuli. Furthermore, NFAT1 translocation into nuclei in CD4 T cells was also significantly promoted by Erdr1 in the presence of TCR stimulation. Taken together, our results indicate that Erdr1 positively modulates TCR signaling strength via enhancing the PLCγ1/Ca2+/NFAT1 signal transduction pathway.

scholarly journals Regulation of positive and negative selection and TCR signaling during thymic T cell development by capicua

2021 ◽  
Author(s):  
Soeun Kim ◽  
Guk-Yeol Park ◽  
Jong Seok Park ◽  
Jiho Park ◽  
Hyebeen Hong ◽  
...  
Keyword(s):  
T Cell ◽  
Negative Selection ◽  
Target Genes ◽  
Selection Process ◽  
T Cell Development ◽  
Cell Development ◽  
Calcium Flux ◽  
Thymic Selection ◽  
Tcr Signaling ◽  
Selection Of

Central tolerance is achieved through positive and negative selection of thymocytes mediated by T cell receptor (TCR) signaling strength. Thus, the dysregulation of the thymic selection process often leads to autoimmunity. Here, we show that capicua (CIC), a transcriptional repressor that suppresses autoimmunity, controls the thymic selection process. Loss of CIC prior to T-cell lineage commitment impaired both positive and negative selection of thymocytes. CIC deficiency attenuated TCR signaling in CD4+CD8+ double-positive (DP) cells, as evidenced by a decrease in CD5 and phospho-ERK levels and calcium flux. We identified Spry4, Dusp4, Dusp6, and Spred1 as CIC target genes that could inhibit TCR signaling in DP cells. Furthermore, impaired positive selection and TCR signaling were partially rescued in Cic and Spry4 double mutant mice. Our findings indicate that CIC is a transcription factor required for thymic T cell development and suggest that CIC acts at multiple stages of T cell development and differentiation to prevent autoimmunity.

Calcium signaling on Jurkat T cells induced by microbeads coated with novel peptide ligands specific to human CD3ε

2021 ◽  
Vol 9 (6) ◽  
pp. 1661-1675
Author(s):  
Armin Ahmadi ◽  
V. S. S. Abhinav Ayyadevara ◽  
Jerome Baudry ◽  
Kyung-Ho Roh
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
Calcium Signaling ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Peptide Ligands ◽  
Calcium Flux ◽  
Tcr Signaling ◽  
Jurkat T Cells ◽  
Magnetic Microbeads

Magnetic microbeads decorated with novel peptide ligands against human CD3ε can activate the Jurkat T cells via specific T cell receptor (TCR) signaling pathways linked to calcium flux, IL-2 secretion, and cell proliferation.

The nuclear 3,5,3'-triiodothyronine receptor in human leukaemic cell lines

1984 ◽  
Vol 105 (3) ◽  
pp. 429-432 ◽  
Author(s):  
Juan Bernal ◽  
Leif C. Andersson
Keyword(s):  
Growth Hormone ◽  
Cell Line ◽  
Cell Lines ◽  
Rat Liver ◽  
Association Constant ◽  
Erythroid Differentiation ◽  
Leukaemic Cell ◽  
Cells In Culture ◽  
Gh Cells ◽  
High Concentrations

Abstract. The 3,5,3'-triiodothyronine (T3) receptor has been studied in a series of continuously growing human leukaemic cell lines. High concentrations of receptor were found in the erythroblastoid cell line K-562. T3 was bound to the nuclei of these cells with an association constant of 3.4 × 109 m−1, and capacity 104 fmol/100 μg DNA, or 8700 molecules/nucleus. This capacity is comparable to that of rat liver or growth hormone producing cells (GH cells) in culture, and suggests that the K-562 cell line could be a useful model for the study of T3 action on erythroid differentiation.

Mislocalization of Adherens Junction- Associated Proteins in a Patient with Darier Disease

2018 ◽  
Vol 2 (3) ◽  
pp. 184-201
Author(s):  
George D Glinos ◽  
Irena Pastar ◽  
Marjana Tomic-Canic ◽  
Rivka C Stone
Keyword(s):  
Adherens Junction ◽  
Cellular Adhesion ◽  
Calcium Flux ◽  
Keratinocyte Differentiation ◽  
Calcium Dependent ◽  
Endoplasmic Reticulum Calcium ◽  
Darier Disease ◽  
Associated Proteins ◽  
Attachment Proteins ◽  
E Cadherin

Darier disease (DD) is an autosomal dominant keratinizing genodermatosis that manifests clinically with red-brown pruritic papules in a seborrheic distribution often in association with palmoplantar pits and dystrophic nail changes. It is caused by mutation in ATP2A2 which encodes a sarco/endoplasmic reticulum calcium ATPase isoform 2 (SERCA2) pump that regulates calcium flux. Consequent alteration of intracellular calcium homeostasis is thought to impair trafficking of cellular adhesion proteins and to lead to aberrant keratinocyte differentiation, contributing to the characteristic histopathologic features of acantholysis and dyskeratosis in DD, though the precise mechanisms are incompletely understood. Previous studies have identified defective localization of desmosomal attachment proteins in skin biopsies and cultured keratinocytes from DD patients, but reports of effects on adherens junction proteins (including calcium-dependent E-cadherin) are conflicting. Here we describe a case of DD presenting with characteristic clinical and histologic features in which we performed immunofluorescence staining of four adherens junction-associated proteins (E-cadherin, α-catenin, β-catenin, and vinculin). In lesional (acantholytic) DD skin, we identified loss of distinctive bright membranous staining that was present at the periphery of keratinocytes throughout the epidermis in the healthy skin of a matched donor. Perilesional (non-acantholytic) portions of DD skin partially recapitulated the normal phenotype. Our findings support a role for SERCA2 dysfunction in impaired assembly of adherens junctions, which together with defective desmosomes contribute to acantholysis in DD.

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