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. 2021 Apr 29;64(7):1626–1641. doi: 10.1007/s00125-021-05453-z

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — TLOs in human donors with type 1 diabetes. (a, b) Representative images of a heavily inflamed (CD45⁺) insulin-positive islet in peri-insulitis stage (donor no. 6325) (a) with intermixed T cells and B cells (b). PLM marks the peri-islet BM, endothelial BM of blood vessels and acinar BM (a) and a consecutive section stained for T cells (CD3⁺), B cells (CD20⁺) and collagen type III shows the RFs (b); boxed area is shown at higher magnification. (c) Representative image of a heavily inflamed islet characterised by disruption of peri-islet BM (PLM⁺) by infiltrating immune cells (CD45⁺). The arrow marks intact peri-islet BM and the arrowhead marks disrupted peri-islet BM; boxed area is shown at higher magnification. (d, e) Visualisation of a heavily inflamed insulin-positive islet with T cell and B cell compartments (donor no. E124B). Collagen VI marks the interstitial matrix of the islet and surrounding exocrine tissue, CD45 labels all leucocytes (d). Immunofluorescence staining for CD3 and CD20 reveals T cell and B cell compartments and MECA79 staining identifies HEVs (arrows) in the T cell zone (e). (f, g) Frequency of TLOs in relation to the age at diabetes diagnosis (f, *p<0.05) and disease duration (g, p=0.3). (h) Proportion of islets with TLOs in relation to disease severity, which was defined by assigning the islets into four phases based on their insulin content and on the presence of insulitis: phase 0 (insulin-positive islets without insulitis); phase 1 (insulin-positive islets with insulitis); phase 2 (insulin-negative islets with insulitis); and phase 3 (insulin-negative islets without insulitis). There was a statistically significant difference across these groups using the Kruskal–Wallis test (***p<0.001). Proportion of islets with TLOs in donors with compartmentalised (TLOs Comp.) and intermixed TLOs (TLOs Int.) (p=0.2) (i). There was no difference in age at diagnosis among donors classified by TLO stages (p=0.1090, Kruskal–Wallis test) (j) but disease duration was different (*p<0.05, Kruskal–Wallis test) (k). Scale bars, 100 μm, or 50 μm for areas of higher magnification. Data are shown as means ± SD in all graphs. Coll, collagen; is, islet