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Diabetes. 2019 Aug;68(8):1544-1551. doi: 10.2337/dbi18-0048.

The Immunoreactive Platform of the Pancreatic Islets Influences the Development of Autoreactivity.

Author information

1
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO unanue@wustl.edu.
2
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO.

Abstract

Tissue homeostasis is maintained through a finely tuned balance between the immune system and the organ-resident cells. Disruption of this process not only results in organ dysfunction but also may trigger detrimental autoimmune responses. The islet of Langerhans consists of the insulin-producing β-cells essential for proper control of body metabolism, but less appreciated is that these cells naturally interact with the immune system, forming a platform by which the β-cell products are sensed, processed, and responded to by the local immune cells, particularly the islet-resident macrophages. Although its physiological outcomes are not completely understood, this immunoreactive platform is crucial for precipitating islet autoreactivity in individuals carrying genetic risks, leading to the development of type 1 diabetes. In this Perspective, we summarize recent studies that examine the cross talk between the β-cells and various immune components, with a primary focus on discussing how antigenic information generated during normal β-cell catabolism can be delivered to the resident macrophage and further recognized by the adaptive CD4 T-cell system, a critical step to initiate autoimmune diabetes. The core nature of the islet immune platform can be extrapolated to other endocrine tissues and may represent a common mechanism underlying the development of autoimmune syndromes influencing multiple endocrine organs.

PMID:
31331989
PMCID:
PMC6692819
[Available on 2020-08-01]
DOI:
10.2337/dbi18-0048

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