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REVIEW article

Front. Immunol.

Sec. Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders

Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1677177

This article is part of the Research TopicThe Role of Innate Immunity in the Pathogenesis of Autoimmune and Autoinflammatory DiseasesView all 4 articles

Sensing Danger in the Islet: The Roles of Pattern Recognition Receptors in β Cells and Type 1 Diabetes

Provisionally accepted
Lixiang  TongLixiang Tong1Yiting  TuYiting Tu2Shoujun  HuangShoujun Huang3*Peilin  ZhengPeilin Zheng1*
  • 1The People's Hospital of Longhua Shenzhen, Shenzhen, China
  • 2Shenzhen Samii International Medical Center, Shenzhen, China
  • 3Anhui Agricultural University, Hefei, China

The final, formatted version of the article will be published soon.

Type 1 diabetes (T1D) is an organ-specific autoimmune disease characterized by the immune-mediated destruction of pancreatic β cells, leading to absolute insulin deficiency and chronic hyperglycemia. Traditionally, the onset of T1D has been attributed to the interplay of genetic predisposition and environmental factors that disrupt immune tolerance. However, growing evidence suggests that β cells are not merely passive targets of immune attack. Instead, under conditions of inflammatory and metabolic stress, β cells actively participate in immune modulation by upregulating various immunologically relevant molecules, particularly pattern recognition receptors (PRRs). These innate immune sensors enable β cells to detect danger-associated signals and modulate local immune responses, thereby influencing their survival and immunogenicity. In this review, we summarize current knowledge about the expression profiles and immunoregulatory roles of PRRs in pancreatic β cells and explore their potential contributions to T1D pathogenesis. A deeper understanding of PRR-mediated signaling in β cells may provide novel insights into the immunopathology of T1D and reveal promising targets for therapeutic intervention.

Keywords: Pattern Recognition Receptors, innate immunity, Pancreatic β cells, type 1 diabetes, Autoimmunity

Received: 31 Jul 2025; Accepted: 25 Aug 2025.

Copyright: © 2025 Tong, Tu, Huang and Zheng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Shoujun Huang, Anhui Agricultural University, Hefei, China
Peilin Zheng, The People's Hospital of Longhua Shenzhen, Shenzhen, China

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