Modulatory role of skin microbiome against UV
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE117359 | GEO | 2019/05/26
REPOSITORIES: GEO
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Project description:Modulatory role of skin microbiome against UV
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Project description:We used a high-throughput sequencing method known as CPD-seq to map the formation of UV-induced cyclobutane pyrimidine dimers (CPD) at single nucleotide resolution in UV-irradiated yeast genomic DNA (naked DNA) in the presence or absence of cytosine methylation at CpG sites by the methyltransferase M.SssI.
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Project description:The exposure of skin to ultraviolet (UV) radiation results in sunburn cell (SBC) and cyclobutane pyrimidine dimer (CPD) formation and local immune suppression. However, the pathways that regulate these events are poorly understood. Here, we exposed mice to UVB to study the early cytotoxic effects in absence of E3 ubiquitin protein ligase Cbl-b. We observed that Cbl-b-/- mice developed significantly less SBCs and CPDs compared to WT mice. In addition, microarray analysis revealed that loss of Cbl-b-induced cell tolerance genes rather than DNA repair genes. Taken together, our results suggest a novel role of Cbl-b in regulating UV cytotoxicity.
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Project description:Our data demonstrate that lung and bone marrow-derived megakaryocytes (Mks) have distinct immune phenotypes and functions; lung Mks secrete inflammatory cytokines and express molecules that are similar to many tissue resident leukocytes and antigen presenting cells (APCs), and lung Mks process live intact bacteria and present bacteria-derived antigen to CD4+ T cells both in vitro and in vivo. Our in vivo data suggest that lung Mks have important roles in the early activation of T cell responses to a pulmonary pathogen challenge, identifying a novel immune regulatory role for lung Mks.
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Project description:AHA labelled peptides in control and UV treated cells in presence and absence of DAC51, SBI56, METTL3 siRNA.
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Project description:UV radiation (UV) alters secondary metabolism in the skin of Vitis vinifera L. berries, which may affect on the final composition of both, grapes and wines. We compared berry skin transcriptome and phenolic composition between Tempranillo berries grown in the presence or absence of solar UV in a mid-altitude Tempranillo vineyard. By analysing two different ripening degrees, expression of 121 genes was significantly altered. Functional enrichment identified that, principally, secondary metabolism-related transcripts were induced by UV, including VvFLS1, VvGT5 and VvGT6 flavonol biosynthetic genes induction. Concurrently, flavonol accumulation was the most evident impact of UV on the berry skin phenolic composition. Monoterpenoid biosynthetic transcripts were also up-regulated by UV, whereas induction of stilbenoid biosynthetic transcripts and stilbenes accumulation was probably induced by the joint action of UV and other condition under the UV-blocking filter, likely higher temperature. Among regulatory genes, VvMYBF1, VvMYB24 and three bHLH transcription factors were up-regulated by UV. Homologs to Arabidopsis UVR8-dependent UV-B-induced genes were also induced, including VvHY5-1, VvHY5-2 and VvRUP UV-B signalling genes. This suggests that the UV-B-specific signalling pathway is activated in the skin of grapes grown at low-medium altitudes. The biosynthesis and accumulation of UV-absorbing compounds that are appreciated for winemaking were almost specifically triggered, which indicates that viticultural practices increasing solar UV incidence may improve grape features important to wine production.
2014-09-09 | GSE54636 | GEO
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Project description:The paper describes a model of interaction of Th cells and macrophage in melanoma.
Created by COPASI 4.25 (Build 207)
This model is described in the article:
Modelling and investigation of the CD4 T cells – Macrophages paradox in melanoma immunotherapies
Raluca Eftimie, Haneen Hamam
Journal of Theoretical Biology 420 (2017) 82–104
Abstract:
It is generally accepted that tumour cells can be eliminated by M1 anti-tumour macrophages and CD8+ T cells. However, experimental results over the past 10–15 years have shown that B16 mouse melanoma cells can be eliminated by the CD4+ T cells alone (either Th1 or Th2 sub-types), in the absence of CD8+ T cells. In some studies, elimination of B16 melanoma was associated with a Th1 immune response (i.e., elimination occurred in the presence of cytokines produced by Th1 cells), while in other studies melanoma elimination was associated with a Th2 immune response (i.e., elimination occurred in the presence of cytokines produced by Th2 cells). Moreover, macrophages have been shown to be present inside the tumours, during both Th1 and Th2 immune responses. To investigate the possible biological mechanisms behind these apparently contradictory results, we develop a class of mathematical models for the dynamics of Th1 and Th2 cells, and M1 and M2 macrophages in the presence/absence of tumour cells. Using this mathematical model, we show that depending on the re- polarisation rates between M1 and M2 macrophages, we obtain tumour elimination in the presence of a type-I immune response (i.e., more Th1 and M1 cells, compared to the Th2 and M2 cells), or in the presence of a type- II immune response (i.e., more Th2 and M2 cells). Moreover, tumour elimination is also possible in the presence of a mixed type-I/type-II immune response. Tumour growth always occurs in the presence of a type-II immune response, as observed experimentally. Finally, tumour dormancy is the result of a delicate balance between the pro-tumour effects of M2 cells and the anti-tumour effects of M1 and Th1 cells.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models .
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide.
Please refer to CC0 Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000769 | BioModels
Project description:The paper describes a model of interaction of Th cells and macrophage in melanoma.
Created by COPASI 4.25 (Build 207)
This model is described in the article:
Modelling and investigation of the CD4 T cells – Macrophages paradox in melanoma immunotherapies
Raluca Eftimie, Haneen Hamam
Journal of Theoretical Biology 420 (2017) 82–104
Abstract:
It is generally accepted that tumour cells can be eliminated by M1 anti-tumour macrophages and CD8+ T cells. However, experimental results over the past 10–15 years have shown that B16 mouse melanoma cells can be eliminated by the CD4+ T cells alone (either Th1 or Th2 sub-types), in the absence of CD8+ T cells. In some studies, elimination of B16 melanoma was associated with a Th1 immune response (i.e., elimination occurred in the presence of cytokines produced by Th1 cells), while in other studies melanoma elimination was associated with a Th2 immune response (i.e., elimination occurred in the presence of cytokines produced by Th2 cells). Moreover, macrophages have been shown to be present inside the tumours, during both Th1 and Th2 immune responses. To investigate the possible biological mechanisms behind these apparently contradictory results, we develop a class of mathematical models for the dynamics of Th1 and Th2 cells, and M1 and M2 macrophages in the presence/absence of tumour cells. Using this mathematical model, we show that depending on the re- polarisation rates between M1 and M2 macrophages, we obtain tumour elimination in the presence of a type-I immune response (i.e., more Th1 and M1 cells, compared to the Th2 and M2 cells), or in the presence of a type- II immune response (i.e., more Th2 and M2 cells). Moreover, tumour elimination is also possible in the presence of a mixed type-I/type-II immune response. Tumour growth always occurs in the presence of a type-II immune response, as observed experimentally. Finally, tumour dormancy is the result of a delicate balance between the pro-tumour effects of M2 cells and the anti-tumour effects of M1 and Th1 cells.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models .
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide.
Please refer to CC0 Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000770 | BioModels