# Tissue Resident and Infiltrating Immune Cells: Their Influence on the Demise of Beta Cells in Type 1 Diabetes

**Authors:** Sophie L. Walker, Pia Leete, Joanne Boldison

PMC · DOI: 10.3390/biom15030441 · Biomolecules · 2025-03-19

## TL;DR

This paper reviews how immune cells in the pancreas contribute to the destruction of insulin-producing cells in type 1 diabetes.

## Contribution

The paper provides a comprehensive review of immune cell interactions in the pancreas during type 1 diabetes progression.

## Key findings

- T1D involves multiple immune cells creating an inflamed pancreatic environment.
- Resident and infiltrating immune cells play roles in beta cell destruction.
- The disease is heterogeneous, with variable rates of beta cell damage.

## Abstract

Type 1 diabetes (T1D) is an organ-specific autoimmune disease that results in the selective loss of pancreatic beta cells and an eventual deficit in insulin production to maintain glucose homeostasis. It is now increasingly accepted that this dynamic disease process is multifactorial; involves a variety of immune cells which contribute to an inflamed pancreatic microenvironment; and that the condition is heterogenous, resulting in variable rates of subsequent beta cell damage. In this review, we will explore the current understanding of the cellular interactions between both resident and infiltrating immune cells within the pancreatic environment, highlighting key mechanisms which may promote the beta cell destruction and islet damage associated with T1D.

## Linked entities

- **Diseases:** Type 1 diabetes (MONDO:0005147), T1D (MONDO:0005147)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** T1D (MESH:D003922), autoimmune disease (MESH:D001327), islet damage (MESH:D007516)

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11939886/full.md

## References

99 references — full list in the complete paper: https://tomesphere.com/paper/PMC11939886/full.md

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Source: https://tomesphere.com/paper/PMC11939886