Category: Current nPOD Projects

Quantitative proteomic profiling of human islets in healthy and diabetes associated pregnancy

Normal pregnancy is associated with a rise in insulin secretion, which begins at placental implantation and increases progressively in parallel with placental growth. Following placenta delivery there is a sharp postpartum decline in insulin secretion. Gestational diabetes (GDM),the development of diabetes for the first time during pregnancy, is associated with pancreatic beta-cell dysfunction. Rodent models […]

Identification of protective niches in T1D pancreata

Type 1 diabetes (T1D) is caused by an autoimmune attack mediated by cytotoxic T cells. However as the attack unfolds, many other cell types participate–and some play an anti-inflammatory, regulatory, role. Interestingly, in the early stages of the disease, attacked islets often reside next to non-attacked islets. We hypothesized that the “tranquil” islets harbor elements […]

Changes in human islet microvasculature during the progression of type 1 diabetes

The pancreatic islet is surrounded by an extracellular matrix (ECM) composed of laminin, collagen IV, and proteoglycans, that support islet function and viability. Type 1 diabetes (T1D) is characterized by the immunemediated loss of insulin-producing β-cells in the islet. Islet infiltration by activated immune cells results in the degradation of the peri-islet ECM eliminating critical […]

Pathogenic Action of Autoantibodies on Islet Function and Viability in Type 1 Diabetes

Type 1 Diabetes (T1D) is known to develop over time when autoimmune processes attack and destroy beta cells thereby reducing the capacity to secrete adequate amounts of insulin. The relatively gradual progression of the disease offers an opportunity for therapeutic intervention to slow or prevent destruction of beta cells before the disease has reached symptomatic […]

Mapping islet B cells in the pancreas on a single-cell level

Recent evidence suggests a role for B cells in the pathogenesis of type 1 diabetes (T1D), particularly in individuals who develop T1D at a younger age and demonstrate rapid progression. However, little is known regarding the specificity, phenotype, and function of B cells in young-onset T1D. Recently we performed a cross-sectional analysis comparing insulin-reactive to […]

Unraveling the Role of CD45RA+CCR7+CD4 T Cells in the Pathogenesis of Type 1 Diabetes

This study aims to investigate the role of CD45RA+CCR7+CD4 T cells in the pathogenesis of type 1 diabetes (T1D). Historically, naïve T cells were deemed irrelevant in T1D development due to their presumed lack of antigen experience. However, distinct subsets of naïve T cells with varying phenotypes and functions have been identified, with recent literature […]

Unbiased single cell resolution spatial proteomics: defining the antigenic landscape in the context of HLA-I expression during type 1 diabetes progression

Diabetes is a complex metabolic disease in which patients experience high blood glucose levels leading to a plethora of symptoms and long-term complications. In type 1 diabetes (T1D), this happens likely due to an autoimmune reaction targeting the insulin producing cell population, so-called beta cells, within the pancreatic islets. CD8+ T-cells are considered the main […]

CD6 and its ligands in Type 1 Diabetes

Type 1 diabetes mellitus (T1D) results from the autoimmune attack of pancreatic β-cells, resulting in a loss of functional β-cell mass. The CD6 molecule is a membrane glycoprotein predominantly expressed on T cells and is implicated in lymphocyte adhesion, activation, and proinflammatory commitment. The CD6 ligand CD166/ALCAM is upregulated in mature dendritic cells and the […]

IAPP and innate immunity in T1D

Islet amyloid polypeptide (IAPP) is a beta-cell peptide hormone that forms toxic and pro-inflammatory aggregates in pathological states, including T2D and islet transplants. Recent evidence suggests the presence of fibrillar aggregates of IAPP (islet amyloid) in some T1D pancreatic islets. In T2D and mouse models of islet amyloid formation, aggregates of human IAPP recruit and […]

Analysis of innate immune response of myeloid cells in human Type 1 diabetes

Type 1 diabetes (T1D) is a multifactorial autoimmune disease that requires genetic susceptibility as well as environmental triggers to induce disease onset. Genetic association studies have implicated the IFIH1 gene, encoding for melanoma differentiation-associated protein 5 (MDA5), a cytosolic sensor of dsRNA, to be involved in T1D susceptibility and resistance. Stimulation of the MDA5 signaling […]

Role of Alpha Cells in Pathogenesis of Type 1 Diabetes

Multiple islet autoantibodies (AAb+) predict type 1 diabetes (T1D) and hyperglycemia within 10 years. By contrast, T1D develops in just ~15% of single AAb+ (generally against glutamic acid decarboxylase, GADA+) individuals; hence the single AAb+ state may represent an early stage of T1D. We previously discovered the functional defects in suppression of glucagon secretion in […]

Congruence of lab versus histopathologic findings of acute pancreatitis in the nPOD consortium

Acute pancreatitis is the cause of more than 200,000 hospital admissions in the United States each year (1). Acute pancreatitis presents very broadly, hence diagnosis can be difficult and requires confirmatory tests. Serum amylase and lipase levels have been established as markers for disease. However, they lack adequate specificity and sensitivity which might make their […]

Stellate cells in type 1 diabetes research (STELLAR)

The loss of insulin-producing β-cells is central to the pathogenesis of type 1 diabetes (T1D). More recently, the contribution of the exocrine pancreatic cellular components is becoming evident in determining the β-cells well-being. Other pancreatic cell types could be acting by reducing β-cell resistance to the autoimmune attack or inducing a stressful condition that will […]

Redoxins in the pathogenesis of type 1 diabetes

We plan to quantify redoxin expression levels and the frequency and type of redoxin expressing pancreatic cells by imaging procedures established in our group. For this purpose we propose a pilot study with samples from #3 cases ideally with rapid (pre-type 1 or type 1 diabetes) or more chronic (type 2 diabetes) ongoing beta cell […]