Sequential pathogenic events in Type 1 Diabetes: Recruitment of Cytotoxic T cells at disease onset

SUMMARY

Type 1 diabetes (T1D) results from the autoimmune destruction of insulin producing b cells, however the complex interactions between islets and cells of the immune system in human patients is poorly described. By performing pseudo time analysis of islets and immune cells using Imaging Mass Cytometry (IMC) through TD1 progression, we provide snapshots to reconstruct the evolution of b cells loss.  In this white paper, we have described an approach using proprietary spatial data analysis to elucidate the association between the immune cells and islet cells in T1D pathogenesis and provides a rationale for designing new therapeutics to cure this disease. 

INTRODUCTION

The pancreas is a highly complex organ consisting of multiple endocrine, exocrine, and stromal cell types and an intricate vascular and neuronal network. In the case of type 1 diabetes (T1D), bidirectional interactions between immune cells and insulin-producing beta cells lead to loss of functional pancreatic beta cell mass and a dependence on exogenous insulin administration for survival. Determining the sequential pathogenic events that take place in the T1D progression in human patients is limited. An understanding of how cell types, cell states, and cell-cell interactions evolve during T1D development is essential to design strategies to cure or halt this disorder. 

In the present study, we characterized the alterations in islet architecture, and immune cell presentation during disease progression. We used Imaging Mass Cytometry (IMC) to investigate complex events on the cellular level and provide new insights on the TD1 pathogenesis. By performing pseudo time analysis, we aim to establish the interaction between the immune system and the endocrine cells and offer an innovative therapeutic approach with a better understanding of events that are critical to the disease pathogenesis.

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