UMMS Affiliation

Division of Diabetes, Department of Medicine, Diabetes Center of Excellence,

Publication Date

2017-07-01

Document Type

Article

Disciplines

Endocrine System Diseases | Endocrinology, Diabetes, and Metabolism | Immune System Diseases | Nutritional and Metabolic Diseases

Abstract

AIMS/HYPOTHESIS: Pancreatic lymph nodes (PLNs) are critical sites for the initial interaction between islet autoantigens and autoreactive lymphocytes, but the histology of PLNs in tissue from individuals with type 1 diabetes has not been analysed in detail. The aim of this study was to examine PLN tissue sections from healthy donors compared with those at risk of, or with recent-onset and longer-duration type 1 diabetes.

METHODS: Immunofluorescence staining was used to examine PLN sections from the following donor groups: non-diabetic (n=15), non-diabetic islet autoantibody-positive (n=5), recent-onset ( < /=1.5 years duration) type 1 diabetes (n=13), and longer-duration type 1 diabetes (n=15). Staining for CD3, CD20 and Ki67 was used to detect primary and secondary (germinal centre-containing) follicles and CD21 and CD35 to detect follicular dendritic cell networks.

RESULTS: The frequency of secondary follicles was lower in the recent-onset type 1 diabetes group compared with the non-diabetic control group. The presence of insulitis (as evidence of ongoing beta cell destruction) and diagnosis of type 1 diabetes at a younger age, however, did not appear to be associated with a lower frequency of secondary follicles. A higher proportion of primary B cell follicles were observed to lack follicular dendritic cell networks in the recent-onset type 1 diabetes group.

CONCLUSIONS/INTERPRETATION: Histological analysis of rare PLNs from individuals with type 1 diabetes suggests a previously unrecognised phenotype comprising decreased primary B cell follicle frequency and fewer follicular dendritic cell networks in recent-onset type 1 diabetes.

Keywords

Histology, Islet autoimmunity, Pancreatic lymph nodes, Type 1 diabetes

Rights and Permissions

© The Author(s) 2017. This article is published with open access at Springerlink.com

DOI of Published Version

10.1007/s00125-017-4221-7

Source

Diabetologia. 2017 Jul;60(7):1294-1303. doi: 10.1007/s00125-017-4221-7. Epub 2017 Feb 17. Link to article on publisher's site

Journal/Book/Conference Title

Diabetologia

Related Resources

Link to Article in PubMed

PubMed ID

28213757

Creative Commons License

Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.

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