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Article ; Online: The MS Remyelinating Drug Bexarotene (an RXR Agonist) Promotes Induction of Human Tregs and Suppresses Th17 Differentiation

Gaunt, Christopher M / Rainbow, Daniel B / Mackenzie, Ruairi J / Jarvis, Lorna B / Mousa, Hani S / Cunniffe, Nicholas / Georgieva, Zoya / Brown, J William / Coles, Alasdair J / Jones, Joanne L

Frontiers in immunology

2021 Volume 12, Page(s) 712241

Abstract: The retinoid X receptor agonist bexarotene promotes remyelination in patients with multiple sclerosis. Murine studies have also demonstrated that RXR agonists have anti-inflammatory effects by enhancing the ability of all-trans-retinoic acid ( ...

Abstract	The retinoid X receptor agonist bexarotene promotes remyelination in patients with multiple sclerosis. Murine studies have also demonstrated that RXR agonists have anti-inflammatory effects by enhancing the ability of all-trans-retinoic acid (
MeSH term(s)	Adult ; Alitretinoin/pharmacology ; Bexarotene/pharmacology ; CD4-Positive T-Lymphocytes/cytology ; CD4-Positive T-Lymphocytes/drug effects ; Cells, Cultured ; Clinical Trials as Topic ; Fatty Acids, Unsaturated/pharmacology ; Female ; Forkhead Transcription Factors/analysis ; Humans ; Leukocytes, Mononuclear/cytology ; Leukocytes, Mononuclear/drug effects ; Lymphopoiesis/drug effects ; Middle Aged ; Remyelination/drug effects ; Retinoid X Receptors/agonists ; Retinoid X Receptors/physiology ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/immunology ; Tetrahydronaphthalenes/pharmacology ; Th17 Cells/cytology ; Th17 Cells/drug effects
Chemical Substances	AGN 194204 ; FOXP3 protein, human ; Fatty Acids, Unsaturated ; Forkhead Transcription Factors ; Retinoid X Receptors ; Tetrahydronaphthalenes ; Alitretinoin (1UA8E65KDZ) ; Bexarotene (A61RXM4375)
Language	English
Publishing date	2021-08-10
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.712241
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Article ; Online: Stochastic search and joint fine-mapping increases accuracy and identifies previously unreported associations in immune-mediated diseases.

Asimit, Jennifer L / Rainbow, Daniel B / Fortune, Mary D / Grinberg, Nastasiya F / Wicker, Linda S / Wallace, Chris

Nature communications

2019 Volume 10, Issue 1, Page(s) 3216

Abstract: Thousands of genetic variants are associated with human disease risk, but linkage disequilibrium (LD) hinders fine-mapping the causal variants. Both lack of power, and joint tagging of two or more distinct causal variants by a single non-causal SNP, lead ...

Abstract	Thousands of genetic variants are associated with human disease risk, but linkage disequilibrium (LD) hinders fine-mapping the causal variants. Both lack of power, and joint tagging of two or more distinct causal variants by a single non-causal SNP, lead to inaccuracies in fine-mapping, with stochastic search more robust than stepwise. We develop a computationally efficient multinomial fine-mapping (MFM) approach that borrows information between diseases in a Bayesian framework. We show that MFM has greater accuracy than single disease analysis when shared causal variants exist, and negligible loss of precision otherwise. MFM analysis of six immune-mediated diseases reveals causal variants undetected in individual disease analysis, including in IL2RA where we confirm functional effects of multiple causal variants using allele-specific expression in sorted CD4
MeSH term(s)	Alleles ; Autoimmunity/genetics ; Bayes Theorem ; CD4-Positive T-Lymphocytes ; CTLA-4 Antigen/genetics ; Chromosome Mapping ; Gene Expression Regulation ; Genetic Association Studies/methods ; Genetic Predisposition to Disease/genetics ; Genome-Wide Association Study/methods ; Genotype ; Humans ; Interleukin-2 Receptor alpha Subunit/genetics ; Linkage Disequilibrium ; Models, Genetic ; Phenotype ; Polymorphism, Single Nucleotide
Chemical Substances	CTLA-4 Antigen ; CTLA4 protein, human ; IL2RA protein, human ; Interleukin-2 Receptor alpha Subunit
Language	English
Publishing date	2019-07-19
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-019-11271-0
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Article: Multimodal profiling reveals tissue-directed signatures of human immune cells altered with age.

Wells, Steven B / Rainbow, Daniel B / Mark, Michal / Szabo, Peter A / Ergen, Can / Maceiras, Ana Raquel / Caron, Daniel P / Rahmani, Elior / Benuck, Eli / Amiri, Valeh Valiollah Pour / Chen, David / Wagner, Allon / Howlett, Sarah K / Jarvis, Lorna B / Ellis, Karen L / Kubota, Masaru / Matsumoto, Rei / Mahbubani, Krishnaa / Saeb-Parsy, Kouresh /

Dominguez-Conde, Cecilia / Richardson, Laura / Xu, Chuan / Li, Shuang / Mamanova, Lira / Bolt, Liam / Wilk, Alicja / Teichmann, Sarah A / Farber, Donna L / Sims, Peter A / Jones, Joanne L / Yosef, Nir

bioRxiv : the preprint server for biology

2024

Abstract: The immune system comprises multiple cell lineages and heterogeneous subsets found in blood and tissues throughout the body. While human immune responses differ between sites and over age, the underlying sources of variation remain unclear as most ... ...

Abstract	The immune system comprises multiple cell lineages and heterogeneous subsets found in blood and tissues throughout the body. While human immune responses differ between sites and over age, the underlying sources of variation remain unclear as most studies are limited to peripheral blood. Here, we took a systems approach to comprehensively profile RNA and surface protein expression of over 1.25 million immune cells isolated from blood, lymphoid organs, and mucosal tissues of 24 organ donors aged 20-75 years. We applied a multimodal classifier to annotate the major immune cell lineages (T cells, B cells, innate lymphoid cells, and myeloid cells) and their corresponding subsets across the body, leveraging probabilistic modeling to define bases for immune variations across donors, tissue, and age. We identified dominant tissue-specific effects on immune cell composition and function across lineages for lymphoid sites, intestines, and blood-rich tissues. Age-associated effects were intrinsic to both lineage and site as manifested by macrophages in mucosal sites, B cells in lymphoid organs, and T and NK cells in blood-rich sites. Our results reveal tissue-specific signatures of immune homeostasis throughout the body and across different ages. This information provides a basis for defining the transcriptional underpinnings of immune variation and potential associations with disease-associated immune pathologies across the human lifespan.
Language	English
Publishing date	2024-01-04
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.03.573877
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Article ; Online: Discovery of CD80 and CD86 as recent activation markers on regulatory T cells by protein-RNA single-cell analysis.

Trzupek, Dominik / Dunstan, Melanie / Cutler, Antony J / Lee, Mercede / Godfrey, Leila / Jarvis, Lorna / Rainbow, Daniel B / Aschenbrenner, Dominik / Jones, Joanne L / Uhlig, Holm H / Wicker, Linda S / Todd, John A / Ferreira, Ricardo C

Genome medicine

2020 Volume 12, Issue 1, Page(s) 55

Abstract: Background: Traditionally, the transcriptomic and proteomic characterisation of CD4: Methods: We have quantified the single-cell expression of 397 genes at the mRNA level and up to 68 proteins using oligo-conjugated antibodies (AbSeq) in 43,656 ... ...

Abstract	Background: Traditionally, the transcriptomic and proteomic characterisation of CD4 Methods: We have quantified the single-cell expression of 397 genes at the mRNA level and up to 68 proteins using oligo-conjugated antibodies (AbSeq) in 43,656 primary CD4 Results: We provide a high-resolution map of human primary CD4 Conclusions: The transcriptomic and proteomic hybrid technology described in this study provides a cost-effective solution to dissect the heterogeneity of immune cell populations at extremely high resolution. Unexpectedly, CD80 and CD86, normally expressed on antigen-presenting cells, were detected on a subset of activated Tregs, indicating a role for these co-stimulatory molecules in regulating the dynamics of CD4
MeSH term(s)	Adolescent ; Adult ; B7-1 Antigen/immunology ; B7-2 Antigen/immunology ; Female ; Forkhead Transcription Factors/genetics ; Humans ; Male ; Proteome ; RNA ; RNA-Seq ; Single-Cell Analysis ; T-Lymphocytes, Regulatory/immunology ; Transcriptome
Chemical Substances	B7-1 Antigen ; B7-2 Antigen ; CD80 protein, human ; CD86 protein, human ; FOXP3 protein, human ; Forkhead Transcription Factors ; Proteome ; RNA (63231-63-0)
Language	English
Publishing date	2020-06-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2484394-5
ISSN	1756-994X ; 1756-994X
ISSN (online)	1756-994X
ISSN	1756-994X
DOI	10.1186/s13073-020-00756-z
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Article: In-depth immunophenotyping data of IL-6R on the human peripheral regulatory T cell (Treg) compartment

Ferreira, Ricardo C. / Rainbow, Daniel B. / Rubio García, Arcadio / Pekalski, Marcin L. / Porter, Linsey / Oliveira, João J. / Waldron-Lynch, Frank / Wicker, Linda S. / Todd, John A.

Data in Brief. 2017 June, v. 12

2017

Abstract: We provide in this paper a detailed characterization of the human peripheral CD4⁺ CD127ˡᵒʷCD25⁺ regulatory T cell (Treg) compartment, with a particular emphasis in defining the population expressing higher levels of the IL-6 receptor (IL-6R). We provide ... ...

Abstract	We provide in this paper a detailed characterization of the human peripheral CD4⁺ CD127ˡᵒʷCD25⁺ regulatory T cell (Treg) compartment, with a particular emphasis in defining the population expressing higher levels of the IL-6 receptor (IL-6R). We provide a description of the phenotype of this population by assessing both the surface expression by flow cytometry as well as their transcriptional profile and functional features. In addition, we also present functional data describing the responsiveness of these subsets to IL-6 signalling in vitro and to IL-2 in vivo. The data presented in this paper support the research article “Human IL-6RʰⁱTIGIT⁻ CD4⁺CD127ˡᵒʷCD25⁺ T cells display potent in vitro suppressive capacity and a distinct Th17 profile” (Ferreira RC et al., 2017; doi: 10.1016/j.clim.2017.03.002) [1].
Keywords	T-lymphocytes ; flow cytometry ; humans ; immunophenotyping ; interleukin-2 ; interleukin-6 ; phenotype ; transcription (genetics)
Language	English
Dates of publication	2017-06
Size	p. 676-691.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	2786545-9
ISSN	2352-3409
ISSN	2352-3409
DOI	10.1016/j.dib.2017.04.043
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Article ; Online: Genetic and functional data identifying Cd101 as a type 1 diabetes (T1D) susceptibility gene in nonobese diabetic (NOD) mice.

Mattner, Jochen / Mohammed, Javid P / Fusakio, Michael E / Giessler, Claudia / Hackstein, Carl-Philipp / Opoka, Robert / Wrage, Marius / Schey, Regina / Clark, Jan / Fraser, Heather I / Rainbow, Daniel B / Wicker, Linda S

PLoS genetics

2019 Volume 15, Issue 6, Page(s) e1008178

Abstract: Type 1 diabetes (T1D) is a chronic multi-factorial disorder characterized by the immune-mediated destruction of insulin-producing pancreatic beta cells. Variations at a large number of genes influence susceptibility to spontaneous autoimmune T1D in non- ... ...

Abstract	Type 1 diabetes (T1D) is a chronic multi-factorial disorder characterized by the immune-mediated destruction of insulin-producing pancreatic beta cells. Variations at a large number of genes influence susceptibility to spontaneous autoimmune T1D in non-obese diabetic (NOD) mice, one of the most frequently studied animal models for human disease. The genetic analysis of these mice allowed the identification of many insulin-dependent diabetes (Idd) loci and candidate genes, one of them being Cd101. CD101 is a heavily glycosylated transmembrane molecule which exhibits negative-costimulatory functions and promotes regulatory T (Treg) function. It is abundantly expressed on subsets of lymphoid and myeloid cells, particularly within the gastrointestinal tract. We have recently reported that the genotype-dependent expression of CD101 correlates with a decreased susceptibility to T1D in NOD.B6 Idd10 congenic mice compared to parental NOD controls. Here we show that the knockout of CD101 within the introgressed B6-derived Idd10 region increased T1D frequency to that of the NOD strain. This loss of protection from T1D was paralleled by decreased Gr1-expressing myeloid cells and FoxP3+ Tregs and an enhanced accumulation of CD4-positive over CD8-positive T lymphocytes in pancreatic tissues. As compared to CD101+/+ NOD.B6 Idd10 donors, adoptive T cell transfers from CD101-/- NOD.B6 Idd10 mice increased T1D frequency in lymphopenic NOD scid and NOD.B6 Idd10 scid recipients. Increased T1D frequency correlated with a more rapid expansion of the transferred CD101-/- T cells and a lower proportion of recipient Gr1-expressing myeloid cells in the pancreatic lymph nodes. Fewer of the Gr1+ cells in the recipients receiving CD101-/- T cells expressed CD101 and the cells had lower levels of IL-10 and TGF-β mRNA. Thus, our results connect the Cd101 haplotype-dependent protection from T1D to an anti-diabetogenic function of CD101-expressing Tregs and Gr1-positive myeloid cells and confirm the identity of Cd101 as Idd10.
MeSH term(s)	Animals ; Antigens, CD/genetics ; Antigens, Ly/genetics ; CD4-Positive T-Lymphocytes/metabolism ; CD8-Positive T-Lymphocytes/metabolism ; Diabetes Mellitus, Type 1/genetics ; Diabetes Mellitus, Type 1/pathology ; Gene Expression Regulation/genetics ; Genetic Predisposition to Disease ; Haplotypes/genetics ; Humans ; Lymph Nodes/metabolism ; Lymph Nodes/pathology ; Mice ; Mice, Inbred NOD ; Mice, Knockout ; Myeloid Cells/immunology ; Myeloid Cells/metabolism ; Pancreas/metabolism ; Pancreas/pathology ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism
Chemical Substances	Antigens, CD ; Antigens, Ly ; Cd101 protein, mouse ; Ly6G antigen, mouse
Language	English
Publishing date	2019-06-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1008178
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Article ; Online: Therapeutically expanded human regulatory T-cells are super-suppressive due to HIF1A induced expression of CD73.

Communications biology

2021 Volume 4, Issue 1, Page(s) 1186

Abstract: The adoptive transfer of regulatory T-cells (Tregs) is a promising therapeutic approach in transplantation and autoimmunity. However, because large cell numbers are needed to achieve a therapeutic effect, in vitro expansion is required. By comparing ... ...

Abstract	The adoptive transfer of regulatory T-cells (Tregs) is a promising therapeutic approach in transplantation and autoimmunity. However, because large cell numbers are needed to achieve a therapeutic effect, in vitro expansion is required. By comparing their function, phenotype and transcriptomic profile against ex vivo Tregs, we demonstrate that expanded human Tregs switch their metabolism to aerobic glycolysis and show enhanced suppressive function through hypoxia-inducible factor 1-alpha (HIF1A) driven acquisition of CD73 expression. In conjunction with CD39, CD73 expression enables expanded Tregs to convert ATP to immunosuppressive adenosine. We conclude that for maximum therapeutic benefit, Treg expansion protocols should be optimised for CD39/CD73 co-expression.
MeSH term(s)	5'-Nucleotidase/genetics ; 5'-Nucleotidase/metabolism ; Female ; GPI-Linked Proteins/genetics ; GPI-Linked Proteins/metabolism ; Gene Expression Regulation ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Male ; T-Lymphocytes, Regulatory/metabolism
Chemical Substances	GPI-Linked Proteins ; HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; 5'-Nucleotidase (EC 3.1.3.5) ; NT5E protein, human (EC 3.1.3.5)
Language	English
Publishing date	2021-10-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-021-02721-x
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Article ; Online: Genome-wide transcriptional analyses of islet-specific CD4+ T cells identify Idd9 genes controlling diabetogenic T cell function.

Berry, Gregory J / Frielle, Christine / Luu, Thaiphi / Salzberg, Anna C / Rainbow, Daniel B / Wicker, Linda S / Waldner, Hanspeter

Journal of immunology (Baltimore, Md. : 1950)

2015 Volume 194, Issue 6, Page(s) 2654–2663

Abstract: Type 1 diabetes (T1D) is a polygenic disease with multiple insulin-dependent diabetes (Idd) loci predisposing humans and NOD mice to disease. NOD.B10 Idd9 congenic mice, in which the NOD Idd9 chromosomal region is replaced by the Idd9 from T1D-resistant ... ...

Abstract	Type 1 diabetes (T1D) is a polygenic disease with multiple insulin-dependent diabetes (Idd) loci predisposing humans and NOD mice to disease. NOD.B10 Idd9 congenic mice, in which the NOD Idd9 chromosomal region is replaced by the Idd9 from T1D-resistant C57BL/10 mice, are significantly protected from T1D development. However, the genes and pathways conferring T1D development or protection by Idd9 remain to be fully elucidated. We have developed novel NOD.B10-Idd9 (line 905) congenic mice that predominantly harbor islet-reactive CD4(+) T cells expressing the BDC2.5 TCR (BDC-Idd9.905 mice). To establish functional links between the Idd9 genotype and its phenotype, we used microarray analyses to investigate the gene expression profiles of ex vivo and Ag-activated CD4(+) T cells from these mice and BDC2.5 (BDC) NOD controls. Among the differentially expressed genes, those located within the Idd9 region were greatly enriched in islet-specific CD4(+) T cells. Bioinformatics analyses of differentially expressed genes between BDC-Idd9.905 and BDC CD4(+) T cells identified Eno1, Rbbp4, and Mtor, all of which are encoded by Idd9 and part of gene networks involved in cellular growth and development. As predicted, proliferation and Th1/Th17 responses of islet-specific CD4(+) T cells from BDC-Idd9.905 mice following Ag stimulation in vitro were reduced compared with BDC mice. Furthermore, proliferative responses to endogenous autoantigen and diabetogenic function were impaired in BDC-Idd9.905 CD4(+) T cells. These findings suggest that differential expression of the identified Idd9 genes contributed to Idd9-dependent T1D susceptibility by controlling the diabetogenic function of islet-specific CD4(+) T cells.
MeSH term(s)	Animals ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; Cell Proliferation/genetics ; Chromosome Mapping ; Chromosomes, Mammalian/genetics ; Cluster Analysis ; Diabetes Mellitus, Type 1/genetics ; Diabetes Mellitus, Type 1/immunology ; Gene Expression Profiling/methods ; Gene Regulatory Networks ; Genetic Predisposition to Disease/genetics ; Genome-Wide Association Study/methods ; Islets of Langerhans/metabolism ; Mice ; Mice, Congenic ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, Transgenic ; Oligonucleotide Array Sequence Analysis ; Phosphopyruvate Hydratase/genetics ; Retinoblastoma-Binding Protein 4/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism
Chemical Substances	Retinoblastoma-Binding Protein 4 ; Phosphopyruvate Hydratase (EC 4.2.1.11)
Language	English
Publishing date	2015-03-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1401288
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Ud II Zs.37: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: The soluble CTLA-4 splice variant protects from type 1 diabetes and potentiates regulatory T-cell function.

Gerold, Kay D / Zheng, Peilin / Rainbow, Daniel B / Zernecke, Alma / Wicker, Linda S / Kissler, Stephan

Diabetes

2011 Volume 60, Issue 7, Page(s) 1955–1963

Abstract: Objective: CTLA4 gene variation associates with multiple autoimmune disorders, including type 1 diabetes. The CTLA4 susceptibility allele was found to generate decreased levels of mRNA encoding soluble CTLA-4 (sCTLA-4) relative to the full-length ... ...

Abstract	Objective: CTLA4 gene variation associates with multiple autoimmune disorders, including type 1 diabetes. The CTLA4 susceptibility allele was found to generate decreased levels of mRNA encoding soluble CTLA-4 (sCTLA-4) relative to the full-length isoform, the functional consequence of which is as yet unknown. In this study, we investigated the contribution of sCTLA-4 to immune regulation with the aim to elucidate the functional basis of the disease association of CTLA4. Research design and methods: To model the disease-associated splicing variation of CTLA4, we generated NOD mice in which sCTLA-4 mRNA is silenced by RNA interference. Results: We found that loss of sCTLA-4 impairs the function of regulatory T (Treg) cells. This functional defect could be attributed, at least in part, to the failure of sCTLA-4 knockdown (KD) Treg cells to downregulate dendritic cell costimulation. sCTLA-4 KD Treg cells, in contrast with wild-type Treg cells, failed to inhibit colitis induced by transfer of CD4(+)CD45RB(hi) cells into NOD.SCID animals. Furthermore, diminished sCTLA-4 expression accelerated the onset of autoimmune diabetes in transgenic mice. Conclusions: Our results demonstrate that sCTLA-4 participates in immune regulation by potentiating the function of Treg cells. The functional outcome of silencing this splice variant in the NOD model provides an explanation for the association of CTLA4 variation with autoimmunity. Lower sCTLA-4 expression from the susceptibility allele may directly affect the suppressive capacity of Treg cells and thereby modulate disease risk. Our unprecedented approach establishes the feasibility of modeling splicing variations relevant to autoimmunity.
MeSH term(s)	Alternative Splicing ; Animals ; Antigens, CD/genetics ; Antigens, CD/physiology ; CTLA-4 Antigen ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/prevention & control ; Gene Knockdown Techniques ; Mice ; Mice, Inbred NOD ; Mice, Transgenic ; Protein Isoforms/genetics ; Protein Isoforms/physiology ; T-Lymphocytes, Regulatory/immunology
Chemical Substances	Antigens, CD ; CTLA-4 Antigen ; Ctla4 protein, mouse ; Protein Isoforms
Language	English
Publishing date	2011-05-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db11-0130
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Article: In-depth immunophenotyping data of IL-6R on the human peripheral regulatory T cell (Treg) compartment.

Ferreira, Ricardo C / Rainbow, Daniel B / Rubio García, Arcadio / Pekalski, Marcin L / Porter, Linsey / Oliveira, João J / Waldron-Lynch, Frank / Wicker, Linda S / Todd, John A

Data in brief

2017 Volume 12, Page(s) 676–691

Abstract: We provide in this paper a detailed characterization of the human peripheral ... ...

Abstract	We provide in this paper a detailed characterization of the human peripheral CD4
Language	English
Publishing date	2017-05-02
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2786545-9
ISSN	2352-3409
ISSN	2352-3409
DOI	10.1016/j.dib.2017.04.043
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