% Refs to be added
@article{Huang2009,
abstract = {DAVID bioinformatics resources consists of an integrated biological knowledgebase and analytic tools aimed at systematically extracting biological meaning from large gene/protein lists. This protocol explains how to use DAVID, a high-throughput and integrated data-mining environment, to analyze gene lists derived from high-throughput genomic experiments. The procedure first requires uploading a gene list containing any number of common gene identifiers followed by analysis using one or more text and pathway-mining tools such as gene functional classification, functional annotation chart or clustering and functional annotation table. By following this protocol, investigators are able to gain an in-depth understanding of the biological themes in lists of genes that are enriched in genome-scale studies.},
author = {Huang, Da Wei and Sherman, Brad T and Lempicki, Richard a},
doi = {10.1038/nprot.2008.211},
issn = {1750-2799},
journal = {Nature Protocols},
keywords = {Computational Biology,Computational Biology: methods,Data Interpretation, Statistical,Genes,Genes: genetics,Genomics,Genomics: methods,Internet,Software},
month = {jan},
number = {1},
pages = {44--57},
pmid = {19131956},
title = {{Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources.}},
url = {http://www.ncbi.nlm.nih.gov/pubmed/19131956},
volume = {4},
year = {2009}
}
@article{Alasoo2018,
abstract = {Regulatory variants are often context specific, modulating gene expression in a subset of possible cellular states. Although these genetic effects can play important roles in disease, the molecular mechanisms underlying context specificity are poorly understood. Here, we identified shared quantitative trait loci (QTLs) for chromatin accessibility and gene expression in human macrophages exposed to IFN$\gamma$, Salmonella and IFN$\gamma$ plus Salmonella. We observed that {\~{}}60{\%} of stimulus-specific expression QTLs with a detectable effect on chromatin altered the chromatin accessibility in naive cells, thus suggesting that they perturb enhancer priming. Such variants probably influence binding of cell-type-specific transcription factors, such as PU.1, which can then indirectly alter the binding of stimulus-specific transcription factors, such as NF-$\kappa$B or STAT2. Thus, although chromatin accessibility assays are powerful for fine-mapping causal regulatory variants, detecting their downstream effects on gene expression will be challenging, requiring profiling of large numbers of stimulated cellular states and time points.},
author = {Alasoo, Kaur and Rodrigues, Julia and Mukhopadhyay, Subhankar and Knights, Andrew J. and Mann, Alice L. and Kundu, Kousik and Hale, Christine and Dougan, Gordon and Gaffney, Daniel J.},
doi = {10.1038/s41588-018-0046-7},
file = {:Users/fede/Library/Containers/com.apple.Preview/Data/Downloads/s41588-018-0046-7.pdf:pdf},
issn = {15461718},
journal = {Nature Genetics},
mendeley-groups = {ideal{\_}manuscript,GeneTonic{\_}manuscript},
number = {3},
pages = {424--431},
publisher = {Springer US},
title = {{Shared genetic effects on chromatin and gene expression indicate a role for enhancer priming in immune response}},
url = {http://dx.doi.org/10.1038/s41588-018-0046-7},
volume = {50},
year = {2018}
}
@article{Love2014,
abstract = {In comparative high-throughput sequencing assays, a fundamental task is the analysis of count data, such as read counts per gene in RNA-seq, for evidence of systematic changes across experimental conditions. Small replicate numbers, discreteness, large dynamic range and the presence of outliers require a suitable statistical approach. We present DESeq2, a method for differential analysis of count data, using shrinkage estimation for dispersions and fold changes to improve stability and interpretability of estimates. This enables a more quantitative analysis focused on the strength rather than the mere presence of differential expression. The DESeq2 package is available at http://www.bioconductor.org/packages/release/bioc/html/DESeq2.html webcite.},
author = {Love, Michael I and Huber, Wolfgang and Anders, Simon},
doi = {10.1186/s13059-014-0550-8},
file = {:Users/fede/Library/Application Support/Mendeley Desktop/Downloaded/Love, Huber, Anders - 2014 - Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2.pdf:pdf},
isbn = {1465-6906},
issn = {1474-760X},
journal = {Genome Biology},
keywords = {Algorithms,Computational Biology,Computational Biology: methods,Genetic,High-Throughput Nucleotide Sequencing,Models,RNA,RNA: analysis,Sequence Analysis,Software},
mendeley-groups = {PhDthesis,pcaExplorer{\_}manuscript,ideal{\_}manuscript,VFapplication,VF,iSEE,GeneTonic{\_}manuscript},
month = {dec},
number = {12},
pages = {550},
pmid = {25516281},
title = {{Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2}},
url = {http://genomebiology.biomedcentral.com/articles/10.1186/s13059-014-0550-8},
volume = {15},
year = {2014}
}
@article{Dutertre2019,
abstract = {Human mononuclear phagocytes comprise phenotypically and functionally overlapping subsets of dendritic cells (DCs) and monocytes, but the extent of their heterogeneity and distinct markers for subset identification remains elusive. By integrating high-dimensional single-cell protein and RNA expression data, we identified distinct markers to delineate monocytes from conventional DC2 (cDC2s). Using CD88 and CD89 for monocytes and HLA-DQ and Fc$\epsilon$RI$\alpha$ for cDC2s allowed for their specific identification in blood and tissues. We also showed that cDC2s could be subdivided into phenotypically and functionally distinct subsets based on CD5, CD163, and CD14 expression, including a distinct subset of circulating inflammatory CD5−CD163+CD14+ cells related to previously defined DC3s. These inflammatory DC3s were expanded in systemic lupus erythematosus patients and correlated with disease activity. These findings further unravel the heterogeneity of DC subpopulations in health and disease and may pave the way for the identification of specific DC subset-targeting therapies. Using high-dimensional protein and RNA single-cell analyses, Dutertre et al. analyze human dendritic cell and monocyte subsets and identify markers that delineate them and unravel their heterogeneity. They also reveal the presence of inflammatory CD14+ DC3s, a subset of cDC2s, that correlate with disease progression and may be functionally involved in systemic lupus erythematosus immunopathology.},
author = {Dutertre, Charles Antoine and Becht, Etienne and Irac, Sergio Erdal and Khalilnezhad, Ahad and Narang, Vipin and Khalilnezhad, Shabnam and Ng, Pei Y. and van den Hoogen, Lucas L. and Leong, Jing Yao and Lee, Bernett and Chevrier, Marion and Zhang, Xiao Meng and Yong, Pearly Jean Ai and Koh, Geraldine and Lum, Josephine and Howland, Shanshan Wu and Mok, Esther and Chen, Jinmiao and Larbi, Anis and Tan, Henry Kun Kiaang and Lim, Tony Kiat Hon and Karagianni, Panagiota and Tzioufas, Athanasios G. and Malleret, Benoit and Brody, Joshua and Albani, Salvatore and van Roon, Joel and Radstake, Timothy and Newell, Evan W. and Ginhoux, Florent},
doi = {10.1016/j.immuni.2019.08.008},
file = {:Users/fede/Downloads/dutertre2019.pdf:pdf},
issn = {10974180},
journal = {Immunity},
keywords = {CD88,CD89,DC2,DC3,Fc$\epsilon$RI$\alpha$,SLE,dendritic cell,inflammatory DC,lupus,monocyte,pre-DC},
number = {3},
pages = {573--589.e8},
pmid = {31474513},
publisher = {Elsevier Inc.},
title = {{Single-Cell Analysis of Human Mononuclear Phagocytes Reveals Subset-Defining Markers and Identifies Circulating Inflammatory Dendritic Cells}},
url = {https://doi.org/10.1016/j.immuni.2019.08.008},
volume = {51},
year = {2019}
}
