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Dr Pia Leete

Post Doctoral Research Fellow

RILD Building

University of Exeter Medical School, RILD Building, RD&E Hospital Wonford, Barrack Road, Exeter, EX2 5DW, UK

Overview

My research group focusses on exploring the multifaceted nature of the immunopathology of Type 1 diabetes in the pancreas.

After a nontraditional career trajectory, I am a current and proud recipient of a Diabetes UK RD Lawrence Fellowship, and also a fierce advocate for the notion that "anything is possible".

My observations have led to the proposal that two distinct forms of Type 1 diabetes exist, and that age at diagnosis is a strongly prognostic factor for identifying which form a person might be experiencing in their pancreas. One form tends to be diagnosed before teenage-hood, and is linked to a more aggressive destruction of beta-cells. Early age at diagnosis has also been linked to more serious outcomes in later life. Conversely, those diagnosed beyond their mid-teens retain more beta-cells yet still absolutely require the life giving insulin therapy if they are to evade diabetic ketoacidisis. My observations in the pancreas have also revealed that these forms, or endotypes of disease, also appear to differ immunologically. These observations may hold a key to understanding how to target individuals to the most effective therapies for maintaining and preserving their health.

Unfortunately, age is not definitive and at present we have very few clinically accessible clues that can inform us precisely what is happening in the pancreas as the insulin producing beta-cells are destroyed. Therefore, further work to understand what drives these pancreatic and immunological differences is critical if we are to leverage enough information to support the development of targeted and patient-specific therapies aiming to improve long-term health for individuals at risk of, or already diagnosed with, Type 1 diabetes.

I have recently been awarded a prestigious RD Lawrence Fellowship by Diabetes UK to advance this work. The research will continue to explore the pancreatic landscapes in health and disease, at different ages and disease durations, and will also include mathematical modelling to understand the aetiology of this impactful condition. There will also be a period of training with Dr Catherine Arden and Professor Jim Shaw at Newcastle University to learn and develop protocols in the UK to employ the “living slice technology” in my work.

Because my research questions focus on the heterogeneity of T1D, I am also expanding my research portfolio to explore patterns of data gathered in population studies and am currently collaborating with Prof Gillespie at the University of Bristol to understand the heritability of age at diagnosis when the condition is found in families who are affected in a multigenerational manner.

I have had the pleasure of developing my career and working alongside members of the IBEx group for 10 years. During this time, I have been fortunate to work in a team that has supported my growth as a professional, scientist and human begin; and as such, I have a deep commitment to supporting new and emerging scientists to experience the same – no matter who they are. As such, I sit on our faculty EDI committee, ECR committee, and am active LGBTQ+ ally.

Additionally, I beleive that understanding our own health empowers us to work with it; and with this deep belief, I am also increasingly embedded in outreach initiatives and engaging with patient involvement and interest groups.

Qualifications

1st class Hons in Human Biosciences
PhD focussed on the Heterogeneity of the Pancreatic pathology in Type 1 diabetes
Fellow of the Higher Education Authority

Awards

RD Lawrence Fellowship (2023-2027)
FHEA Fellowship
11 Above and Beyond Awards (University of Exeter)
Excellence in Biology (University of Plymouth)

Research group links

Department of Clinical and Biomedical Sciences

Islet Biology Group website

www.isletbiologyexeter.com

Qualifications

1st class Hons in Human Bioscience
PhD focussed on the Heterogeneity of the Pancreatic pathology in T1D
Fellow of the Higher Education Authority

Research group links

Institute of Biomedical and Clinical Science

Research

Publications

Key publications | Publications by category | Publications by year

Publications by category

Journal articles

Leete P, Oram R, McDonald T, Ziller C, Hattersley A, Richardson S, Morgan N (In Press). Studies of insulin and proinsulin in pancreas and serum support the existence of aetiopathological endotypes of type 1 diabetes associated with age at diagnosis. Diabetologia

Ifie E, Russell M, Dhayal S, Leete P, Sebastiani G, Nigi L, Dotta F, Marjomäki V, Eizirik D, Morgan N, et al (In Press). Unexpected subcellular distribution of a specific isoform of the Coxsackie and adenovirus receptor, CAR-SIV, in human pancreatic beta cells. Diabetologia

Boldison J, Hopkinson JR, Davies J, Pearson JA, Leete P, Richardson S, Morgan NG, Wong FS (2023). Gene expression profiling in NOD mice reveals that B cells are highly educated by the pancreatic environment during autoimmune diabetes. Diabetologia, 66(3), 551-566. Abstract.

Carr ALJ, Inshaw JRJ, Flaxman CS, Leete P, Wyatt RC, Russell LA, Palmer M, Prasolov D, Worthington T, Hull B, et al (2022). Circulating C-Peptide Levels in Living Children and Young People and Pancreatic β-Cell Loss in Pancreas Donors Across Type 1 Diabetes Disease Duration. Diabetes, 71(7), 1591-1596. Abstract.

Krogvold L, Leete P, Mynarek IM, Russell MA, Gerling IC, Lenchik NI, Mathews C, Richardson SJ, Morgan NG, Dahl-Jørgensen K, et al (2022). Detection of Antiviral Tissue Responses and Increased Cell Stress in the Pancreatic Islets of Newly Diagnosed Type 1 Diabetes Patients: Results from the DiViD Study. Frontiers in Endocrinology, 13

Aims/hypothesisThe Diabetes Virus Detection (DiViD) study has suggested the presence of low-grade enteroviral infection in pancreatic tissue collected from six of six live adult patients newly diagnosed with type 1 diabetes. The present study aimed to compare the gene and protein expression of selected virally induced pathogen recognition receptors and interferon stimulated genes in islets from these newly diagnosed type 1 diabetes (DiViD) subjects vs age-matched non-diabetic (ND) controls.MethodsRNA was extracted from laser-captured islets and Affymetrix Human Gene 2.0 ST arrays used to obtain gene expression profiles. Lists of differentially expressed genes were subjected to a data-mining pipeline searching for enrichment of canonical pathways, KEGG pathways, Gene Ontologies, transcription factor binding sites and other upstream regulators. In addition, the presence and localisation of specific viral response proteins (PKR, MxA and MDA5) were examined by combined immunofluorescent labelling in sections of pancreatic tissue.ResultsThe data analysis and data mining process revealed a significant enrichment of gene ontologies covering viral reproduction and infectious cycles; peptide translation, elongation and initiation, as well as oxidoreductase activity. Enrichment was identified in the KEGG pathways for oxidative phosphorylation; ribosomal and metabolic activity; antigen processing and presentation and in canonical pathways for mitochondrial dysfunction, oxidative phosphorylation and EIF2 signaling. Protein Kinase R (PKR) expression did not differ between newly diagnosed type 1 diabetes and ND islets at the level of total RNA, but a small subset of β-cells displayed markedly increased PKR protein levels. These PKR+ β-cells correspond to those previously shown to contain the viral protein, VP1. RNA encoding MDA5 was increased significantly in newly diagnosed type 1 diabetes islets, and immunostaining of MDA5 protein was seen in α- and certain β-cells in both newly diagnosed type 1 diabetes and ND islets, but the expression was increased in β-cells in type 1 diabetes. In addition, an uncharacterised subset of synaptophysin positive, but islet hormone negative, cells expressed intense MDA5 staining and these were more prevalent in DiViD cases. MxA RNA was upregulated in newly diagnosed type 1 diabetes vs ND islets and MxA protein was detected exclusively in newly diagnosed type 1 diabetes β-cells.Conclusion/interpretationThe gene expression signatures reveal that pathways associated with cellular stress and increased immunological activity are enhanced in islets from newly diagnosed type 1 diabetes patients compared to controls. The increases in viral response proteins seen in β-cells in newly diagnosed type 1 diabetes provide clear evidence for the activation of IFN signalling pathways. As such, these data strengthen the hypothesis that an enteroviral infection of islet β-cells contributes to the pathogenesis of type 1 diabetes.

Abstract.

Rodriguez-Calvo T, Chen Y-C, Verchere CB, Haataja L, Arvan P, Leete P, Richardson SJ, Morgan NG, Qian W-J, Pugliese A, et al (2021). Altered β-Cell Prohormone Processing and Secretion in Type 1 Diabetes. Diabetes, 70(5), 1038-1050. Abstract. Author URL.

Leete P, Morgan NG (2021). Footprints of Immune Cells in the Pancreas in Type 1 Diabetes; to "B" or Not to "B": is That Still the Question?. Front Endocrinol (Lausanne), 12 Abstract. Author URL.

Russell M, Leete P (2019). Glucocorticoids: novel agents to stimulate beta-cell neogenesis?. Annals of Translational Medicine, 7(8).

Russell MA, Redick SD, Blodgett DM, Richardson SJ, Leete P, Krogvold L, Dahl-Jørgensen K, Bottino R, Brissova M, Spaeth JM, et al (2019). HLA Class II Antigen Processing and Presentation Pathway Components Demonstrated by Transcriptome and Protein Analyses of Islet β-Cells from Donors with Type 1 Diabetes. Diabetes, 68(5), 988-1001. Abstract. Author URL.

Vecchio F, Lo Buono N, Stabilini A, Nigi L, Dufort MJ, Geyer S, Rancoita PM, Cugnata F, Mandelli A, Valle A, et al (2018). Abnormal neutrophil signature in the blood and pancreas of presymptomatic and symptomatic type 1 diabetes. JCI Insight, 3(18).

BACKGROUND: Neutrophils and their inflammatory mediators are key pathogenic components in multiple autoimmune diseases, while their role in human type 1 diabetes (T1D), a disease that progresses sequentially through identifiable stages prior to the clinical onset, is not well understood. We previously reported that the number of circulating neutrophils is reduced in patients with T1D and in presymptomatic at-risk subjects. The aim of the present work was to identify possible changes in circulating and pancreas-residing neutrophils throughout the disease course to better elucidate neutrophil involvement in human T1D. METHODS: Data collected from 389 subjects at risk of developing T1D, and enrolled in 4 distinct studies performed by TrialNet, were analyzed with comprehensive statistical approaches to determine whether the number of circulating neutrophils correlates with pancreas function. To obtain a broad analysis of pancreas-infiltrating neutrophils throughout all disease stages, pancreas sections collected worldwide from 4 different cohorts (i.e. nPOD, DiViD, Siena, and Exeter) were analyzed by immunohistochemistry and immunofluorescence. Finally, circulating neutrophils were purified from unrelated nondiabetic subjects and donors at various T1D stages and their transcriptomic signature was determined by RNA sequencing. RESULTS: Here, we show that the decline in β cell function is greatest in individuals with the lowest peripheral neutrophil numbers. Neutrophils infiltrate the pancreas prior to the onset of symptoms and they continue to do so as the disease progresses. of interest, a fraction of these pancreas-infiltrating neutrophils also extrudes neutrophil extracellular traps (NETs), suggesting a tissue-specific pathogenic role. Whole-transcriptome analysis of purified blood neutrophils revealed a unique molecular signature that is distinguished by an overabundance of IFN-associated genes; despite being healthy, said signature is already present in T1D-autoantibody-negative at-risk subjects. CONCLUSIONS: These results reveal an unexpected abnormality in neutrophil disposition both in the circulation and in the pancreas of presymptomatic and symptomatic T1D subjects, implying that targeting neutrophils might represent a previously unrecognized therapeutic modality. FUNDING: Juvenile Diabetes Research Foundation (JDRF), NIH, Diabetes UK.

Abstract. Author URL.

Shields B, McDonald T, Oram R, Hill A, Hudson M, Leete P, Pearson E, Richardson S, Morgan N, Hattersley A, et al (2018). C-peptide decline in type 1 diabetes has two phases: an initial exponential fall and a subsequent stable phase. Diabetes Care

Colli ML, Hill JLE, Marroquí L, Chaffey J, Dos Santos RS, Leete P, Coomans de Brachène A, Paula FMM, Op de Beeck A, Castela A, et al (2018). PDL1 is expressed in the islets of people with type 1 diabetes and is up-regulated by interferons-α and-γ via IRF1 induction. EBioMedicine, 36, 367-375. Abstract. Author URL.

Leete P, Mallone R, Richardson SJ, Sosenko JM, Redondo MJ, Evans-Molina C (2018). The Effect of Age on the Progression and Severity of Type 1 Diabetes: Potential Effects on Disease Mechanisms. Current Diabetes Reports, 18(11). Abstract.

Hodik M, Anagandula M, Fuxe J, Krogvold L, Dahl-Jørgensen K, Hyöty H, Sarmiento L, Frisk G, Atkinson M, Pugliese A, et al (2016). Coxsackie-adenovirus receptor expression is enhanced in pancreas from patients with type 1 diabetes. BMJ Open Diabetes Research and Care, 4(1). Abstract.

Leete P, Willcox A, Krogvold L, Dahl-Jørgensen K, Foulis AK, Richardson SJ, Morgan NG (2016). Differential Insulitic Profiles Determine the Extent of β-Cell Destruction and the Age at Onset of Type 1 Diabetes. Diabetes, 65(5), 1362-1369. Abstract. Author URL.

Richardson SJ, Rodriguez-Calvo T, Gerling IC, Mathews CE, Kaddis JS, Russell MA, Zeissler M, Leete P, Krogvold L, Dahl-Jørgensen K, et al (2016). Islet cell hyperexpression of HLA class I antigens: a defining feature in type 1 diabetes. Diabetologia, 59(11), 2448-2458.

AIMS/HYPOTHESIS: Human pancreatic beta cells may be complicit in their own demise in type 1 diabetes, but how this occurs remains unclear. One potentially contributing factor is hyperexpression of HLA class I antigens. This was first described approximately 30 years ago, but has never been fully characterised and was recently challenged as artefactual. Therefore, we investigated HLA class I expression at the protein and RNA levels in pancreases from three cohorts of patients with type 1 diabetes. The principal aims were to consider whether HLA class I hyperexpression is artefactual and, if not, to determine the factors driving it. METHODS: Pancreas samples from type 1 diabetes patients with residual insulin-containing islets (n = 26) from the Network for Pancreatic Organ donors with Diabetes (nPOD), Diabetes Virus Detection study (DiViD) and UK recent-onset type 1 diabetes collections were immunostained for HLA class I isoforms, signal transducer and activator of transcription 1 (STAT1), NLR family CARD domain containing 5 (NLRC5) and islet hormones. RNA was extracted from islets isolated by laser-capture microdissection from nPOD and DiViD samples and analysed using gene-expression arrays. RESULTS: Hyperexpression of HLA class I was observed in the insulin-containing islets of type 1 diabetes patients from all three tissue collections, and was confirmed at both the RNA and protein levels. The expression of β2-microglobulin (a second component required for the generation of functional HLA class I complexes) was also elevated. Both 'classical' HLA class I isoforms (i.e. HLA-ABC) as well as a 'non-classical' HLA molecule, HLA-F, were hyperexpressed in insulin-containing islets. This hyperexpression did not correlate with detectable upregulation of the transcriptional regulator NLRC5. However, it was strongly associated with increased STAT1 expression in all three cohorts. Islet hyperexpression of HLA class I molecules occurred in the insulin-containing islets of patients with recent-onset type 1 diabetes and was also detectable in many patients with disease duration of up to 11 years, declining thereafter. CONCLUSIONS/INTERPRETATION: Islet cell HLA class I hyperexpression is not an artefact, but is a hallmark in the immunopathogenesis of type 1 diabetes. The response is closely associated with elevated expression of STAT1 and, together, these occur uniquely in patients with type 1 diabetes, thereby contributing to their selective susceptibility to autoimmune-mediated destruction.

Abstract. Author URL.

Krogvold L, Edwin B, Buanes T, Frisk G, Skog O, Anagandula M, Korsgren O, Undlien D, Eike MC, Richardson SJ, et al (2015). Detection of a low-grade enteroviral infection in the islets of langerhans of living patients newly diagnosed with type 1 diabetes. Diabetes, 64(5), 1682-1687. Abstract. Author URL.

Guy C, Arif S, Leete P, Nguyen V, Marks K, Nor NM, Estorninho M, Kronenberg-Versteeg D, Bingley PJ, Todd JA, et al (2015). Erratum. Blood and Islet Phenotypes Indicate Immunological Heterogeneity in Type 1 Diabetes. Diabetes 2014;63:3835-3845. Diabetes, 64(9). Author URL.

Leete P, Richardson SJ, Krogvold L, Willcox A, Dahl-Jorgensen K, Foulis AK, Morgan NG (2015). Low B-lymphocyte numbers within the insulitic lesion correlates with an elevated proportion of persisting beta cells and later onset of disease in patients with Type 1 diabetes. DIABETIC MEDICINE, 32, 63-63. Author URL.

Arif S, Leete P, Nguyen V, Marks K, Nor NM, Estorninho M, Kronenberg-Versteeg D, Bingley PJ, Todd JA, Guy C, et al (2014). Blood and islet phenotypes indicate immunological heterogeneity in type 1 diabetes. Diabetes, 63(11), 3835-3845. Abstract. Author URL.

Richardson SJ, Leete P, Dhayal S, Russell MA, Oikarinen M, Laiho JE, Svedin E, Lind K, Rosenling T, Chapman N, et al (2014). Detection of enterovirus in the islet cells of patients with type 1 diabetes: what do we learn from immunohistochemistry? Reply to Hansson SF, Korsgren S, Pontén F et al [letter]. Diabetologia, 57(3), 647-649. Author URL.

Leete P, Richardson SJ, Bone AJ, Foulis AK, Morgan NG (2014). Differential expression of anti-apoptotic B-cell lymphoma-2 (Bcl-2) family proteins by the islet endocrine cell subtypes in human pancreas. DIABETIC MEDICINE, 31, 47-48. Author URL.

Richardson SJ, Leete P, Dhayal S, Russell MA, Oikarinen M, Laiho JE, Svedin E, Lind K, Rosenling T, Chapman N, et al (2014). Evaluation of the fidelity of immunolabelling obtained with clone 5D8/1, a monoclonal antibody directed against the enteroviral capsid protein, VP1, in human pancreas. Diabetologia, 57(2), 392-401. Abstract. Author URL.

Morgan NG, Leete P, Foulis AK, Richardson SJ (2014). Islet inflammation in human type 1 diabetes mellitus. IUBMB Life, 66(11), 723-734. Abstract. Author URL.

Richardson SJ, Leete P, Bone AJ, Foulis AK, Morgan NG (2013). Expression of the enteroviral capsid protein VP1 in the islet cells of patients with type 1 diabetes is associated with induction of protein kinase R and downregulation of Mcl-1. Diabetologia, 56(1), 185-193. Abstract. Author URL.

Lind K, Richardson SJ, Leete P, Morgan NG, Korsgren O, Flodström-Tullberg M (2013). Induction of an Antiviral State and Attenuated Coxsackievirus Replication in Type III Interferon Treated Primary Human Pancreatic Islets. Journal of virology

Publications by year

In Press

2023

2022

Abstract.

Boldison J, Hopkinson J, Davies J, Pearson JA, Leete P, Richardson S, Morgan NG, Wong FS (2022). Gene expression profiling reveals B cells are highly educated by the pancreatic environment during autoimmune diabetes.

2021

2019

Russell M, Leete P (2019). Glucocorticoids: novel agents to stimulate beta-cell neogenesis?. Annals of Translational Medicine, 7(8).

2018

Abstract. Author URL.

2016

Abstract. Author URL.

2015

2014

Morgan NG, Leete P, Foulis AK, Richardson SJ (2014). Islet inflammation in human type 1 diabetes mellitus. IUBMB Life, 66(11), 723-734. Abstract. Author URL.

2013

Pia_Leete Details from cache as at 2023-03-30 20:53:25

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Teaching

Supervision / Group

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Dr Pia Leete

Post Doctoral Research Fellow

Overview

Qualifications

Research group links

Research

Publications

Publications by category

Journal articles

Abstract:Gene expression profiling in NOD mice reveals that B cells are highly educated by the pancreatic environment during autoimmune diabetes

Abstract:Circulating C-Peptide Levels in Living Children and Young People and Pancreatic β-Cell Loss in Pancreas Donors Across Type 1 Diabetes Disease Duration

Abstract:Detection of Antiviral Tissue Responses and Increased Cell Stress in the Pancreatic Islets of Newly Diagnosed Type 1 Diabetes Patients: Results from the DiViD Study

Abstract:Altered β-Cell Prohormone Processing and Secretion in Type 1 Diabetes.

Abstract:Footprints of Immune Cells in the Pancreas in Type 1 Diabetes; to "B" or Not to "B": is That Still the Question?

Abstract:HLA Class II Antigen Processing and Presentation Pathway Components Demonstrated by Transcriptome and Protein Analyses of Islet β-Cells from Donors with Type 1 Diabetes.

Abstract:Abnormal neutrophil signature in the blood and pancreas of presymptomatic and symptomatic type 1 diabetes.

Abstract:PDL1 is expressed in the islets of people with type 1 diabetes and is up-regulated by interferons-α and-γ via IRF1 induction.

Abstract:The Effect of Age on the Progression and Severity of Type 1 Diabetes: Potential Effects on Disease Mechanisms

Abstract:Coxsackie-adenovirus receptor expression is enhanced in pancreas from patients with type 1 diabetes

Abstract:Differential Insulitic Profiles Determine the Extent of β-Cell Destruction and the Age at Onset of Type 1 Diabetes.

Abstract:Islet cell hyperexpression of HLA class I antigens: a defining feature in type 1 diabetes.

Abstract:Detection of a low-grade enteroviral infection in the islets of langerhans of living patients newly diagnosed with type 1 diabetes.

Abstract:Blood and islet phenotypes indicate immunological heterogeneity in type 1 diabetes.

Abstract:Evaluation of the fidelity of immunolabelling obtained with clone 5D8/1, a monoclonal antibody directed against the enteroviral capsid protein, VP1, in human pancreas.

Abstract:Islet inflammation in human type 1 diabetes mellitus.

Abstract:Expression of the enteroviral capsid protein VP1 in the islet cells of patients with type 1 diabetes is associated with induction of protein kinase R and downregulation of Mcl-1.

Publications by year

In Press

2023

Abstract:Gene expression profiling in NOD mice reveals that B cells are highly educated by the pancreatic environment during autoimmune diabetes

2022

Abstract:Circulating C-Peptide Levels in Living Children and Young People and Pancreatic β-Cell Loss in Pancreas Donors Across Type 1 Diabetes Disease Duration

Abstract:Detection of Antiviral Tissue Responses and Increased Cell Stress in the Pancreatic Islets of Newly Diagnosed Type 1 Diabetes Patients: Results from the DiViD Study

2021

Abstract:Altered β-Cell Prohormone Processing and Secretion in Type 1 Diabetes.

Abstract:Footprints of Immune Cells in the Pancreas in Type 1 Diabetes; to "B" or Not to "B": is That Still the Question?

2019

Abstract:HLA Class II Antigen Processing and Presentation Pathway Components Demonstrated by Transcriptome and Protein Analyses of Islet β-Cells from Donors with Type 1 Diabetes.

2018

Abstract:Abnormal neutrophil signature in the blood and pancreas of presymptomatic and symptomatic type 1 diabetes.

Abstract:PDL1 is expressed in the islets of people with type 1 diabetes and is up-regulated by interferons-α and-γ via IRF1 induction.

Abstract:The Effect of Age on the Progression and Severity of Type 1 Diabetes: Potential Effects on Disease Mechanisms

2016

Abstract:Coxsackie-adenovirus receptor expression is enhanced in pancreas from patients with type 1 diabetes

Abstract:Differential Insulitic Profiles Determine the Extent of β-Cell Destruction and the Age at Onset of Type 1 Diabetes.

Abstract:Islet cell hyperexpression of HLA class I antigens: a defining feature in type 1 diabetes.

2015

Abstract:Detection of a low-grade enteroviral infection in the islets of langerhans of living patients newly diagnosed with type 1 diabetes.

2014

Abstract:Blood and islet phenotypes indicate immunological heterogeneity in type 1 diabetes.

Abstract:Evaluation of the fidelity of immunolabelling obtained with clone 5D8/1, a monoclonal antibody directed against the enteroviral capsid protein, VP1, in human pancreas.

Abstract:Islet inflammation in human type 1 diabetes mellitus.

2013

Abstract:Expression of the enteroviral capsid protein VP1 in the islet cells of patients with type 1 diabetes is associated with induction of protein kinase R and downregulation of Mcl-1.

Teaching

Supervision / Group

Abstract:
Gene expression profiling in NOD mice reveals that B cells are highly educated by the pancreatic environment during autoimmune diabetes

Abstract:
Circulating C-Peptide Levels in Living Children and Young People and Pancreatic β-Cell Loss in Pancreas Donors Across Type 1 Diabetes Disease Duration

Abstract:
Detection of Antiviral Tissue Responses and Increased Cell Stress in the Pancreatic Islets of Newly Diagnosed Type 1 Diabetes Patients: Results from the DiViD Study

Abstract:
Altered β-Cell Prohormone Processing and Secretion in Type 1 Diabetes.

Abstract:
Footprints of Immune Cells in the Pancreas in Type 1 Diabetes; to "B" or Not to "B": is That Still the Question?

Abstract:
HLA Class II Antigen Processing and Presentation Pathway Components Demonstrated by Transcriptome and Protein Analyses of Islet β-Cells from Donors with Type 1 Diabetes.

Abstract:
Abnormal neutrophil signature in the blood and pancreas of presymptomatic and symptomatic type 1 diabetes.

Abstract:
PDL1 is expressed in the islets of people with type 1 diabetes and is up-regulated by interferons-α and-γ via IRF1 induction.

Abstract:
The Effect of Age on the Progression and Severity of Type 1 Diabetes: Potential Effects on Disease Mechanisms

Abstract:
Coxsackie-adenovirus receptor expression is enhanced in pancreas from patients with type 1 diabetes

Abstract:
Differential Insulitic Profiles Determine the Extent of β-Cell Destruction and the Age at Onset of Type 1 Diabetes.

Abstract:
Islet cell hyperexpression of HLA class I antigens: a defining feature in type 1 diabetes.

Abstract:
Detection of a low-grade enteroviral infection in the islets of langerhans of living patients newly diagnosed with type 1 diabetes.

Abstract:
Blood and islet phenotypes indicate immunological heterogeneity in type 1 diabetes.

Abstract:
Evaluation of the fidelity of immunolabelling obtained with clone 5D8/1, a monoclonal antibody directed against the enteroviral capsid protein, VP1, in human pancreas.

Abstract:
Islet inflammation in human type 1 diabetes mellitus.

Abstract:
Expression of the enteroviral capsid protein VP1 in the islet cells of patients with type 1 diabetes is associated with induction of protein kinase R and downregulation of Mcl-1.

Abstract:
Gene expression profiling in NOD mice reveals that B cells are highly educated by the pancreatic environment during autoimmune diabetes

Abstract:
Circulating C-Peptide Levels in Living Children and Young People and Pancreatic β-Cell Loss in Pancreas Donors Across Type 1 Diabetes Disease Duration

Abstract:
Detection of Antiviral Tissue Responses and Increased Cell Stress in the Pancreatic Islets of Newly Diagnosed Type 1 Diabetes Patients: Results from the DiViD Study

Abstract:
Altered β-Cell Prohormone Processing and Secretion in Type 1 Diabetes.

Abstract:
Footprints of Immune Cells in the Pancreas in Type 1 Diabetes; to "B" or Not to "B": is That Still the Question?

Abstract:
HLA Class II Antigen Processing and Presentation Pathway Components Demonstrated by Transcriptome and Protein Analyses of Islet β-Cells from Donors with Type 1 Diabetes.

Abstract:
Abnormal neutrophil signature in the blood and pancreas of presymptomatic and symptomatic type 1 diabetes.

Abstract:
PDL1 is expressed in the islets of people with type 1 diabetes and is up-regulated by interferons-α and-γ via IRF1 induction.

Abstract:
The Effect of Age on the Progression and Severity of Type 1 Diabetes: Potential Effects on Disease Mechanisms

Abstract:
Coxsackie-adenovirus receptor expression is enhanced in pancreas from patients with type 1 diabetes

Abstract:
Differential Insulitic Profiles Determine the Extent of β-Cell Destruction and the Age at Onset of Type 1 Diabetes.

Abstract:
Islet cell hyperexpression of HLA class I antigens: a defining feature in type 1 diabetes.

Abstract:
Detection of a low-grade enteroviral infection in the islets of langerhans of living patients newly diagnosed with type 1 diabetes.

Abstract:
Blood and islet phenotypes indicate immunological heterogeneity in type 1 diabetes.

Abstract:
Evaluation of the fidelity of immunolabelling obtained with clone 5D8/1, a monoclonal antibody directed against the enteroviral capsid protein, VP1, in human pancreas.

Abstract:
Islet inflammation in human type 1 diabetes mellitus.

Abstract:
Expression of the enteroviral capsid protein VP1 in the islet cells of patients with type 1 diabetes is associated with induction of protein kinase R and downregulation of Mcl-1.