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Article ; Online: Islet beta-cells and intercellular adhesion molecule-1 (ICAM-1): Integrating immune responses that influence autoimmunity and graft rejection.

Martin, Thomas M / Burke, Susan J / Wasserfall, Clive H / Collier, J Jason

2023 Volume 22, Issue 10, Page(s) 103414

Abstract: Type 1 diabetes (T1D) develops due to autoimmune targeting of the pancreatic islet β-cells. Clinical symptoms arise from reduced insulin in circulation. The molecular events and interactions between discrete immune cell populations, infiltration of such ... ...

Abstract	Type 1 diabetes (T1D) develops due to autoimmune targeting of the pancreatic islet β-cells. Clinical symptoms arise from reduced insulin in circulation. The molecular events and interactions between discrete immune cell populations, infiltration of such leukocytes into pancreatic and islet tissue, and selective targeting of the islet β-cells during autoimmunity and graft rejection are not entirely understood. One protein central to antigen presentation, priming of immune cells, trafficking of leukocytes, and vital for leukocyte effector function is the intercellular adhesion molecule-1 (ICAM-1). The gene encoding ICAM-1 is transcriptionally regulated and rapidly responsive (i.e., within hours) to pro-inflammatory cytokines. ICAM-1 is a transmembrane protein that can be glycosylated; its presence on the cell surface provides co-stimulatory functions for immune cell activation and stabilization of cell-cell contacts. ICAM-1 interacts with the β2-integrins, CD11a/CD18 (LFA-1) and CD11b/CD18 (Mac-1), which are present on discrete immune cell populations. A whole-body ICAM-1 deletion protects NOD mice from diabetes onset, strongly implicating this protein in autoimmune responses. Since several different cell types express ICAM-1, its biology is fundamentally essential for various physiological and pathological outcomes. Herein, we review the role of ICAM-1 during both autoimmunity and islet graft rejection to understand the mechanism(s) leading to islet β-cell death and dysfunction that results in insufficient circulating quantities of insulin to control glucose homeostasis.
MeSH term(s)	Animals ; Humans ; Mice ; Autoimmunity ; Graft Rejection ; Insulins ; Intercellular Adhesion Molecule-1/genetics ; Intercellular Adhesion Molecule-1/metabolism ; Islets of Langerhans/metabolism ; Lymphocyte Function-Associated Antigen-1/metabolism ; Macrophage-1 Antigen/metabolism ; Mice, Inbred NOD
Chemical Substances	Insulins ; Intercellular Adhesion Molecule-1 (126547-89-5) ; Lymphocyte Function-Associated Antigen-1 ; Macrophage-1 Antigen ; ICAM1 protein, human
Language	English
Publishing date	2023-08-22
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2144145-5
ISSN	1873-0183 ; 1568-9972
ISSN (online)	1873-0183
ISSN	1568-9972
DOI	10.1016/j.autrev.2023.103414
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Article ; Online: Membrane marker selection for segmenting single cell spatial proteomics data.

Dayao, Monica T / Brusko, Maigan / Wasserfall, Clive / Bar-Joseph, Ziv

Nature communications

2022 Volume 13, Issue 1, Page(s) 1999

Abstract: The ability to profile spatial proteomics at the single cell level enables the study of cell types, their spatial distribution, and interactions in several tissues and conditions. Current methods for cell segmentation in such studies rely on known ... ...

Abstract	The ability to profile spatial proteomics at the single cell level enables the study of cell types, their spatial distribution, and interactions in several tissues and conditions. Current methods for cell segmentation in such studies rely on known membrane or cell boundary markers. However, for many tissues, an optimal set of markers is not known, and even within a tissue, different cell types may express different markers. Here we present RAMCES, a method that uses a convolutional neural network to learn the optimal markers for a new sample and outputs a weighted combination of the selected markers for segmentation. Testing RAMCES on several existing datasets indicates that it correctly identifies cell boundary markers, improving on methods that rely on a single marker or those that extend nuclei segmentations. Application to new spatial proteomics data demonstrates its usefulness for accurately assigning cell types based on the proteins expressed in segmented cells.
MeSH term(s)	Cell Nucleus ; Image Processing, Computer-Assisted/methods ; Neural Networks, Computer ; Proteomics
Language	English
Publishing date	2022-04-14
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-29667-w
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Article ; Online: Optimizing multiplexed imaging experimental design through tissue spatial segregation estimation.

Bost, Pierre / Schulz, Daniel / Engler, Stefanie / Wasserfall, Clive / Bodenmiller, Bernd

Nature methods

2022 Volume 20, Issue 3, Page(s) 418–423

Abstract: Recent advances in multiplexed imaging methods allow simultaneous detection of dozens of proteins and hundreds of RNAs, enabling deep spatial characterization of both healthy and diseased tissues. Parameters for the design of optimal multiplex imaging ... ...

Abstract	Recent advances in multiplexed imaging methods allow simultaneous detection of dozens of proteins and hundreds of RNAs, enabling deep spatial characterization of both healthy and diseased tissues. Parameters for the design of optimal multiplex imaging studies, especially those estimating how much area has to be imaged to capture all cell phenotype clusters, are lacking. Here, using a spatial transcriptomic atlas of healthy and tumor human tissues, we developed a statistical framework that determines the number and area of fields of view necessary to accurately identify all cell phenotypes that are part of a tissue. Using this strategy on imaging mass cytometry data, we identified a measurement of tissue spatial segregation that enables optimal experimental design. This strategy will enable an improved design of multiplexed imaging studies.
MeSH term(s)	Humans ; Research Design ; Diagnostic Imaging ; RNA ; Neoplasms/diagnostic imaging
Chemical Substances	RNA (63231-63-0)
Language	English
Publishing date	2022-12-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2169522-2
ISSN	1548-7105 ; 1548-7091
ISSN (online)	1548-7105
ISSN	1548-7091
DOI	10.1038/s41592-022-01692-z
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Article ; Online: Exocrine and Endocrine Inflammation Increases Cellular Replication in the Pancreatic Duct Compartment in Type 1 Diabetes.

Kulkarni, Shweta / Posgai, Amanda L / Kusmartseva, Irina / Wasserfall, Clive H / Atkinson, Mark A / Butler, Alexandra E

Journal of the Endocrine Society

2022 Volume 6, Issue 11, Page(s) bvac136

Abstract: Context: We recently demonstrated increased cellular proliferation in the pancreatic ductal gland (PDG) compartment of organ donors with type 1 diabetes, suggesting that PDGs may harbor progenitor cells capable of pancreatic regeneration.: Objective: ...

Abstract	Context: We recently demonstrated increased cellular proliferation in the pancreatic ductal gland (PDG) compartment of organ donors with type 1 diabetes, suggesting that PDGs may harbor progenitor cells capable of pancreatic regeneration. Objective: We evaluated the impact of diabetes and pancreatic inflammation on PDG and interlobular duct (ILD) cellular proliferation and profiles. Methods: Endocrine hormone expression (insulin, glucagon, somatostatin, pancreatic polypeptide) and proliferating Ki67+ cells were localized within the PDG and ILD compartments by multicolor immunohistochemistry in cross-sections from the head, body, and tail regions of pancreata from those with (n = 31) or without type 1 diabetes (n = 43). Whole-slide scanned images were analyzed using digital pathology. Results: Type 1 diabetes donors with insulitis or histologically identified pancreatitis had increased cellular replication in the ILD and PDG compartments. Interestingly, while cellular proliferation within the pancreatic ductal tree was significantly increased in type 1 diabetes (PDG mean = 3.36%, SEM = 1.06; ILD mean = 2.78%, SEM = 0.97) vs nondiabetes(ND) subjects without pancreatic inflammation (PDG mean = 1.18%, SEM = 0.42; ILD mean = 0.74%, SEM = 0.15, Conclusion: These data suggest that increased pancreatic ductal cell replication is associated with sustained pancreatic inflammation; however, as replicating cells were hormone-negative, PDGs do not appear to represent a compelling endogenous source of hormone-positive endocrine cells.
Language	English
Publishing date	2022-09-03
Publishing country	United States
Document type	Journal Article
ISSN	2472-1972
ISSN (online)	2472-1972
DOI	10.1210/jendso/bvac136
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Article: Footprint of pancreas infiltrating and circulating immune cells throughout type 1 diabetes development.

Bruggeman, Ylke / Martens, Pieter-Jan / Sassi, Gabriele / Viaene, Marijke / Wasserfall, Clive H / Mathieu, Chantal / Gysemans, Conny

Frontiers in endocrinology

2023 Volume 14, Page(s) 1275316

Abstract: Introduction: Type 1 diabetes (T1D) is defined by immune cell infiltration of the pancreas, in particular the islets of Langerhans, referred to as insulitis, which is especially prominent during the early disease stages in association with decreased ... ...

Abstract	Introduction: Type 1 diabetes (T1D) is defined by immune cell infiltration of the pancreas, in particular the islets of Langerhans, referred to as insulitis, which is especially prominent during the early disease stages in association with decreased beta cell mass. An in-depth understanding of the dynamics and phenotype of the immune cells infiltrating the pancreas and the accompanying changes in their profiles in peripheral blood during T1D development is critical to generate novel preventive and therapeutic approaches, as well as to find biomarkers for the disease process. Methods: Using multi-parameter flow cytometry, we explored the dynamic changes of immune cells infiltrating the pancreas and the pancreatic draining lymph nodes (PLN), compared to those in peripheral blood in female and male non-obese diabetic (NOD) mice during T1D progression. Results: The early stages of T1D development were characterized by an influx of innate dendritic cells and neutrophils in the pancreas. While dendritic cells seemed to move in and out (to the PLN), neutrophils accumulated during the pre-symptomatic phase and reached a maximum at 8 weeks of age, after which their numbers declined. During disease progression, CD4 Conclusion: These time- and tissue-dependent changes in the dynamics and functional states of CD4
MeSH term(s)	Mice ; Animals ; Female ; Male ; Diabetes Mellitus, Type 1/genetics ; CD8-Positive T-Lymphocytes ; Mice, Inbred NOD ; Pancreas/metabolism ; Insulin/metabolism
Chemical Substances	Insulin
Language	English
Publishing date	2023-11-10
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2023.1275316
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Article: Impaired islet function with normal exocrine enzyme secretion is consistent across the head, body, and tail pancreas regions in type 1 diabetes.

Drotar, Denise M / Mojica-Avila, Ana Karen / Bloss, Drew T / Cohrs, Christian M / Manson, Cameron T / Posgai, Amanda L / Williams, MacKenzie D / Brusko, Maigan A / Phelps, Edward A / Wasserfall, Clive H / Speier, Stephan / Atkinson, Mark A

bioRxiv : the preprint server for biology

2024

Abstract: Histopathological heterogeneity in human pancreas has been well documented; however, functional evidence at the tissue level is scarce. Herein we ... ...

Abstract	Histopathological heterogeneity in human pancreas has been well documented; however, functional evidence at the tissue level is scarce. Herein we investigated
Language	English
Publishing date	2024-02-12
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.02.08.579175
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Article ; Online: Serum from pregnant donors induces human beta cell proliferation.

Sylvester-Armstrong, Kendra R / Reeder, Callie F / Powell, Andrece / Becker, Matthew W / Hagan, D Walker / Chen, Jing / Mathews, Clayton E / Wasserfall, Clive H / Atkinson, Mark A / Egerman, Robert / Phelps, Edward A

Islets

2024 Volume 16, Issue 1, Page(s) 2334044

Abstract: Pancreatic beta cells are among the slowest replicating cells in the human body and have not been observed to increase in number except during the fetal and neonatal period, in cases of obesity, during puberty, as well as during pregnancy. Pregnancy is ... ...

Abstract	Pancreatic beta cells are among the slowest replicating cells in the human body and have not been observed to increase in number except during the fetal and neonatal period, in cases of obesity, during puberty, as well as during pregnancy. Pregnancy is associated with increased beta cell mass to meet heightened insulin demands. This phenomenon raises the intriguing possibility that factors present in the serum of pregnant individuals may stimulate beta cell proliferation and offer insights into expansion of the beta cell mass for treatment and prevention of diabetes. The primary objective of this study was to test the hypothesis that serum from pregnant donors contains bioactive factors capable of inducing human beta cell proliferation. An immortalized human beta cell line with protracted replication (EndoC-βH1) was cultured in media supplemented with serum from pregnant and non-pregnant female and male donors and assessed for differences in proliferation. This experiment was followed by assessment of proliferation of primary human beta cells. Sera from five out of six pregnant donors induced a significant increase in the proliferation rate of EndoC-βH1 cells. Pooled serum from the cohort of pregnant donors also increased the rate of proliferation in primary human beta cells. This study demonstrates that serum from pregnant donors stimulates human beta cell proliferation. These findings suggest the existence of pregnancy-associated factors that can offer novel avenues for beta cell regeneration and diabetes prevention strategies. Further research is warranted to elucidate the specific factors responsible for this effect.
MeSH term(s)	Infant, Newborn ; Humans ; Male ; Female ; Pregnancy ; Insulin/metabolism ; Insulin-Secreting Cells/metabolism ; Cell Line ; Diabetes Mellitus/metabolism ; Cell Proliferation
Chemical Substances	Insulin
Language	English
Publishing date	2024-03-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2589489-4
ISSN	1938-2022 ; 1938-2022
ISSN (online)	1938-2022
ISSN	1938-2022
DOI	10.1080/19382014.2024.2334044
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Article ; Online: An antigen-specific immunotherapeutic, AKS-107, deletes insulin-specific B cells and prevents murine autoimmune diabetes.

Alleva, David G / Delpero, Andrea R / Sathiyaseelan, Thillainaygam / Murikipudi, Sylaja / Lancaster, Thomas M / Atkinson, Mark A / Wasserfall, Clive H / Yu, Liping / Ragupathy, Ramya / Bonami, Rachel H / Zion, Todd C

Frontiers in immunology

2024 Volume 15, Page(s) 1367514

Abstract: Introduction: The antigen-presenting cell function of insulin-reactive B cells promotes type 1 diabetes (T1D) in non-obese diabetic (NOD) mice by stimulating pathogenic T cells leading to destruction of insulin-producing β-cells of pancreatic islets.: ...

Abstract	Introduction: The antigen-presenting cell function of insulin-reactive B cells promotes type 1 diabetes (T1D) in non-obese diabetic (NOD) mice by stimulating pathogenic T cells leading to destruction of insulin-producing β-cells of pancreatic islets. Methods/results: To target insulin-reactive B cells, AKS-107, a human IgG1 Fc molecule fused with human insulin A and B chains, was engineered to retain conformational insulin epitopes that bound mouse and human B cell receptors but prevented binding to the insulin metabolic receptor. AKS-107 Fc-mediated deletion of insulin-reactive B cells was demonstrated Discussion: These preclinical outcomes position AKS-107 for clinical development in T1D prevention settings.
MeSH term(s)	Mice ; Animals ; Humans ; Diabetes Mellitus, Type 1 ; Mice, Inbred NOD ; Islets of Langerhans ; B-Lymphocytes ; Mice, Transgenic ; Receptors, Antigen, B-Cell ; Immunotherapy
Chemical Substances	Receptors, Antigen, B-Cell
Language	English
Publishing date	2024-03-07
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2024.1367514
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Article ; Online: Exploration of autoantibody responses in canine diabetes using protein arrays.

O'Kell, Allison L / Shome, Mahasish / Qiu, Ji / Williams, Stacy / Chung, Yunro / LaBaer, Joshua / Atkinson, Mark A / Wasserfall, Clive

Scientific reports

2022 Volume 12, Issue 1, Page(s) 2490

Abstract: Canine diabetes has been considered a potential model of human type 1 diabetes (T1D), however the detection of autoantibodies common in humans with T1D in affected dogs is inconsistent. The aim of this study was to compare autoantibody responses in ... ...

Abstract	Canine diabetes has been considered a potential model of human type 1 diabetes (T1D), however the detection of autoantibodies common in humans with T1D in affected dogs is inconsistent. The aim of this study was to compare autoantibody responses in diabetic and healthy control dogs using a novel nucleic acid programmable protein array (NAPPA) platform. We performed a cross-sectional study of autoantibody profiles of 30 diabetic and 30 healthy control dogs of various breeds. Seventeen hundred human proteins related to the pancreas or diabetes were displayed on NAPPA arrays and interrogated with canine sera. The median normalized intensity (MNI) for each protein was calculated, and results were compared between groups to identify candidate autoantibodies. At a specificity of 90%, six autoantibodies had sensitivity greater than 10% (range 13-20%) for distinguishing diabetic and control groups. A combination of three antibodies (anti-KANK2, anti-GLI1, anti-SUMO2) resulted in a sensitivity of 37% (95% confidence interval (CI) 0.17-0.67%) at 90% specificity and an area under the receiver operating characteristics curve of 0.66 (95% CI 0.52-0.80). While this study does not provide conclusive support for autoimmunity as an underlying cause of diabetes in dogs, future studies should consider the use of canine specific proteins in larger numbers of dogs of breeds at high risk for diabetes.
MeSH term(s)	Animals ; Autoantibodies/blood ; Biomarkers/blood ; Breeding ; Cross-Sectional Studies ; Diabetes Mellitus, Type 1/diagnosis ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/veterinary ; Disease Models, Animal ; Dog Diseases/immunology ; Dogs ; Protein Array Analysis/methods ; ROC Curve ; Risk ; Sensitivity and Specificity
Chemical Substances	Autoantibodies ; Biomarkers
Language	English
Publishing date	2022-02-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-06599-5
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Article ; Online: DNA Methylation-Based Assessment of Cell Composition in Human Pancreas and Islets.

Drawshy, Zeina / Neiman, Daniel / Fridlich, Ori / Peretz, Ayelet / Magenheim, Judith / Rozo, Andrea V / Doliba, Nicolai M / Stoffers, Doris A / Kaestner, Klaus H / Schatz, Desmond A / Wasserfall, Clive / Campbell-Thompson, Martha / Shapiro, James / Kaplan, Tommy / Shemer, Ruth / Glaser, Benjamin / Klochendler, Agnes / Dor, Yuval

Diabetes

2024 Volume 73, Issue 4, Page(s) 554–564

MeSH term(s)	Humans ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Islets of Langerhans/metabolism ; DNA Methylation ; Pancreas/metabolism ; Insulin/metabolism ; Insulin-Secreting Cells/metabolism ; Glucagon-Secreting Cells/metabolism
Chemical Substances	Insulin
Language	English
Publishing date	2024-01-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db23-0704
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