Cellular Origins and Genetic Landscape of Cutaneous Gamma Delta T Cell Lymphoma
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PROVIDER: PRJNA604053 | ENA |
REPOSITORIES: ENA
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Project description:Cellular Origins and Genetic Landscape of Cutaneous Gamma Delta T Cell Lymphoma
| PRJNA604054 | ENA
Project description:We performed gene expression profiling in 34 peripheral T-cell lymphoma, including 7 cases of gamma delta T-cell lymphoma to identify a unique T-cell receptor signature gene set for classification of gamma delta T-cell lymphoma and alpha beta T-cell lymphoma.
2008-10-15 | GSE11946 | GEO
Project description:Background: Malignant clones of primary cutaneous T-cell lymphomas (CTCL) can show a CD4+, CD8+ or T-cell receptor γδ+ phenotype, but their individual impact on tumor biology and skin lesion formation remains ill-defined. We perform a comprehensive molecular characterization of CD4+ vs. CD8+ and TCR-γ/δ+ CTCL lesions. Methods: We performed scRNA-seq of 18 CTCL skin biopsies to compare classic CD4+ advanced-stage mycosis fungoides (MF) with TCR-γ/δ+ MF and primary cutaneous CD8+ aggressive epidermotropic cytotoxic T-cell lymphoma (Berti’s lymphoma). Results: Malignant clones of TCR-γ/δ+ MF and Berti’s lymphoma showed similar clustering patterns distinct from CD4+ MF, along with increased expression of cytotoxic markers such as NKG7, CTSW, GZMA, and GZMM. Only advanced-stage CD4+MF clones expressed central memory T-cell markers (SELL, CCR7, LEF1), alongside B1/B2 blood involvement, whereas TCR-γ/δ+ MF and Berti’s lymphoma harbored a more tissue-resident phenotype (CD69, CXCR4, NR4A1) without detectable cells in the blood. CD4+ MF and TCR-γ/δ+ MF skin lesions harbored strong type 2 immune activation across myeloid cells, while Berti’s lymphoma was more skewed towards type 1 immune responses. Both CD4+ MF and TCR-γ/δ+ MF lesions showed upregulation of keratinocyte hyperactivation markers such as S100As and KRT16 genes. This increase was entirely absent in Berti’s lymphoma, possibly reflecting an aberrant keratinocyte response to invading tumor cells, that could contribute to the formation of the typical ulcero-necrotic lesions within this entity. Conclusions: Our scRNAseq profiling study reveals specific molecular patterns associated with distinct CTCL subtypes.
2024-10-24 | GSE266862 | GEO
Project description:The contribution of chronic antigen stimulation to the occurrence of lymphoproliferative disorder (LPD) with the gamma-delta T-cell lineage is unclear, despite the fact that Epstein-Barr virus (EBV) positive T-cell LPD is derived from antigen-stimulated cytotoxic T-cells. Given the possible association of antigen stimulation with the development of cytotoxic T-cell LPD, we compared gene expression patterns in Epstein-Barr virus (EBV)-positive gamma-delta T-cell lines derived from patients with nasal T-cell lymphoma and chronic active EBV infection and those in gamma-delta T-cells from healthy volunteers. Three EBV-positive gamma-delta T-cells lines, SNT cells (SNT-8, SNT-13 and SNT-15), were used in this study. SNT-8 was established from patients with nasal T-cell lymphoma and SNT-13, -15 were established from patients with chronic active EBV infection (Zhang Y, et al., Br J Cancer 94:599-608, 2006). All the SNT cells exhibits common rearrangement of Vgamma9-JgammaP and Jdelta3 genes. The gamma-delta T-cells obtained from healthy volunteers were expanded ex vivo by 1 microM of zoledronate (ZOL) plus IL-2 for 14 days incubation.
2009-12-09 | GSE13906 | GEO
Project description:The contribution of chronic antigen stimulation to the occurrence of lymphoproliferative disorder (LPD) with the gamma-delta T-cell lineage is unclear, despite the fact that Epstein-Barr virus (EBV) positive T-cell LPD is derived from antigen-stimulated cytotoxic T-cells. Given the possible association of antigen stimulation with the development of cytotoxic T-cell LPD, we compared gene expression patterns in Epstein-Barr virus (EBV)-positive gamma-delta T-cell lines derived from patients with nasal T-cell lymphoma and chronic active EBV infection and those in gamma-delta T-cells from healthy volunteers. Three EBV-positive gamma-delta T-cells lines, SNT cells (SNT-8, SNT-13 and SNT-15), were used in this study. SNT-8 was established from patients with nasal T-cell lymphoma and SNT-13, -15 were established from patients with chronic active EBV infection (Zhang Y, et al., Br J Cancer 94:599-608, 2006). All the SNT cells exhibits common rearrangement of Vgamma9-JgammaP and Jdelta3 genes. The gamma-delta T-cells obtained from healthy volunteers were expanded ex vivo by 1 microM of zoledronate (ZOL) plus IL-2 for 14 days incubation. Experiment Overall Design: We compared gene expression profiling in 3 EBV-positive positive gamma-delta T-cells lines with those in gamma-delta T cells obtaied from a healthy volunteer. Global gene expression was analyzed using the Affymetrix Human Genome U133 2.0 Plus GeneChip Set. Analysis of variance (ANOVA) was done using GeneSifter® (VizXLabs). Values of P<0.05 were considered to be a statistically significant difference.
2009-12-18 | E-GEOD-13906 | biostudies-arrayexpress
Project description:Epithelial cells provide an initial line of defense against damage and pathogens in barrier tissues such as the skin; however this balance is disrupted in obesity and metabolic disease. Skin gamma delta T cells recognize epithelial damage and release cytokines and growth factors that facilitate wound repair. To determine the impact of obesity and metabolic disease on skin gamma delta T cells, we isolated skin gamma delta T cells from 10-week old C57BLKS/J lean db/+ and obese db/db animals for further study. Due to a deficiency in the leptin receptor (db), homozygous db/db animals do not process satiety signals, continually eat and develop severe obesity and metabolic disease. Skin gamma delta T cells isolated from these animals were compared for changes in mRNA expression using microarray. We have determined that obesity and metabolic disease negatively impacts homeostasis and functionality of skin gamma delta T cells, rendering host defense mechanisms vulnerable to injury and infection. The goal of this experiment was to compare skin gamma delta T cells in a control mouse to skin gamma delta T cells isolated from an obese mouse to see what homeostatic changes occur in obesity and metabolic disease. gamma delta T cells were isolated from two 10-week old lean db/+ control and two 10-week old obese db/db animals for comparison. We wanted to determine which growth factors and signaling pathways were altered in skin gamma delta T cells residing in the obese environment.
2010-07-30 | E-GEOD-22196 | biostudies-arrayexpress
Project description:Epithelial cells provide an initial line of defense against damage and pathogens in barrier tissues such as the skin; however this balance is disrupted in obesity and metabolic disease. Skin gamma delta T cells recognize epithelial damage and release cytokines and growth factors that facilitate wound repair. To determine the impact of obesity and metabolic disease on skin gamma delta T cells, we isolated skin gamma delta T cells from 10-week old C57BLKS/J lean db/+ and obese db/db animals for further study. Due to a deficiency in the leptin receptor (db), homozygous db/db animals do not process satiety signals, continually eat and develop severe obesity and metabolic disease. Skin gamma delta T cells isolated from these animals were compared for changes in mRNA expression using microarray. We have determined that obesity and metabolic disease negatively impacts homeostasis and functionality of skin gamma delta T cells, rendering host defense mechanisms vulnerable to injury and infection.
2010-07-01 | GSE22196 | GEO
Project description:T cells bearing gamma delta T cell antigen receptors (TCRs) function in lymphoid stress surveillance. However, the contribution of gamma delta TCRs to such responses is unclear. Here we found that the TCR of a human V gamma4Vdelta5 clone directly bound endothelial protein C receptor (EPCR), which allowed gamma delta T cells to recognize both endothelial cells targeted by cytomegalovirus and epithelial tumors. EPCR is a major histocompatibility complex–like molecule that binds lipids analogously to the antigen-presenting molecule CD1d. However, the V gamma4Vdelta5 TCR bound EPCR independently of lipids, in an antibody-like way. Moreover, the recognition of target cells by gamma delta T cells required a multimolecular stress signature composed of EPCR and costimulatory ligand(s). Our results demonstrate how a gamma delta TCR mediates recognition of broadly stressed human cells by engaging a stress-regulated self antigen.
2012-07-28 | GSE39709 | GEO
Project description:Study of cutaneous biology of cutaneous T cell lymphoma
| PRJNA785680 | ENA
Project description:Study of cutaneous biology of cutaneous T cell lymphoma
| PRJNA785707 | ENA