Insulitis and lymphoid structures in the islets of Langerhans of a 66-year-old patient with long-standing type 1 diabete
- PDF / 9,881,358 Bytes
- 6 Pages / 595.276 x 790.866 pts Page_size
- 112 Downloads / 156 Views
BRIEF REPORT
Insulitis and lymphoid structures in the islets of Langerhans of a 66-year-old patient with long-standing type 1 diabetes Silke Smeets 1 & Willem Staels 2,3,4 & Geert Stangé 1 & Pieter Gillard 1,5 & Nico De Leu 2,6 & Peter in’t Veld 1 Received: 2 April 2020 / Revised: 13 August 2020 / Accepted: 17 August 2020 # The Author(s) 2020
Abstract Insulitis is a characteristic inflammatory lesion consisting of immune cell infiltrates around and within the pancreatic islets of patients with recent-onset type 1 diabetes (T1D). The infiltration is typically mild, both in terms of the number of infiltrating cells and the number of islets affected. Here, we present an unusual histopathological case study of a 66-year-old female patient with long-standing T1D, insulitis, and islet-associated lymphoid tissue. Most islets in the head of the pancreas of this patient were insulin-deficient, whereas the islets in the tail appeared normal. Insulitis was present in 0.84% of the insulin-containing islets and three islets had large lymphocytic infiltrates resembling tertiary lymphoid structures (TLS). Of note, this is the first description of potential TLS in the endocrine pancreas of a patient with T1D. Their association with a marked residual beta cell mass is of interest and may hint at new insights into disease progression and regulation of autoimmunity. Keywords Human . Type 1 diabetes . Insulitis . Pancreas . Tertiary lymphoid structure
Abbreviations T1D Type 1 diabetes TLS Tertiary lymphoid structures
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00428-020-02915-4) contains supplementary material, which is available to authorized users. * Peter in’t Veld [email protected] 1
Diabetes Research Center, Vrije Universiteit Brussel (VUB), Brussels, Belgium
2
Beta Cell Neogenesis (BENE), Vrije Universiteit Brussel (VUB), Brussels, Belgium
3
Institut Cochin, INSERM, U1016, CNRS, UMR8104, Université de Paris, 75014 Paris, France
4
Department of Pediatrics, Division of Pediatric Endocrinology, University Hospital of Brussels, Jette, Belgium
5
Department of Endocrinology, University Hospital Leuven, Leuven, Belgium
6
Department of Endocrinology, UZ Brussel, Brussels, Belgium
Introduction Type 1 diabetes (T1D) is considered to be caused by an autoimmune T cell–mediated destruction of insulin-producing beta cells in the pancreas leading to loss of glucose homeostasis [1]. At disease onset, most pancreatic islets have lost their normal beta cell complement but some still contain insulin. Islets with residual beta cells may show insulitis, a characteristic leucocytic infiltration rich in CD8+ T cells thought to mediate beta cell–specific autoimmunity [2, 3]. Mechanisms of autoimmune beta cell destruction have mainly been studied in animal models, especially that of the non-obese diabetic (NOD) mouse since the disease course in the latter shows many similarities with human T1D. Several important differences, however, exist between the NOD mouse model and patients, inc
Data Loading...
