{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T20:32:02Z","timestamp":1786480322610,"version":"build-2736575974"},"reference-count":58,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","license":[{"start":{"date-parts":[[2025,8,14]],"date-time":"2025-08-14T00:00:00Z","timestamp":1755129600000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001067","name":"Juvenile Diabetes Research Foundation Australia","doi-asserted-by":"crossref","award":["1-SRA-2020-972-M-N"],"award-info":[{"award-number":["1-SRA-2020-972-M-N"]}],"id":[{"id":"10.13039\/501100001067","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100001067","name":"Juvenile Diabetes Research Foundation Australia","doi-asserted-by":"crossref","award":["1-SRA-2020-972-M-N"],"award-info":[{"award-number":["1-SRA-2020-972-M-N"]}],"id":[{"id":"10.13039\/501100001067","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Kidney360"],"published-print":{"date-parts":[[2026,3]]},"abstract":"<jats:sec>\n                    <jats:title>Key Points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Regulatory T cells (Tregs) from people (control, type 1 diabetes with and without albuminuria) were profiled for phenotypic and transcriptomic changes.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            Central memory Tregs were reduced, while Treg EMRA\n                            <jats:sup>+<\/jats:sup>\n                            cells were higher in type 1 diabetes with albuminuria.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            <jats:italic toggle=\"yes\">In silico<\/jats:italic>\n                            findings suggest potential interactions between Treg ligand and kidney cell receptor at transcript level.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Diabetic kidney disease (DKD) is a common complication of type 1 diabetes (T1D). T1D and some kidney disorders are often associated with abnormalities in regulatory T cells (Tregs). However, it is unknown if Treg subsets and their molecular architecture are altered during the onset and progression of DKD in T1D.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We addressed this critical knowledge gap by characterizing changes in Tregs isolated from 31 participants (10 control, 13 with T1D, and eight T1D with albuminuria) using flow cytometry, RNA-sequencing, and microRNA profiling.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We identified that the effector and central memory Tregs were significantly different between groups. Similarly, multiple gene transcripts were also significantly different between groups that also overlapped with other publicly available datasets. Machine learning\u2013based data analyses discovered a set of important microRNAs associated with clinical eGFR values. Importantly, our analyses identified two differentially expressed Treg ligand genes (leucine rich repeat containing 4B, transglutaminase-2), which interacted with the receptors on kidney cells (protein tyrosine phosphatase receptor type D\/F\/S, Adhesion G Protein-Coupled Receptor G1; a.k.a GPR56)\n                      <jats:italic toggle=\"yes\">in silico<\/jats:italic>\n                      , providing potential mechanistic insights into the role of Tregs in DKD progression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Together, our work supports the yet unappreciated role of Tregs in DKD and opens new research avenues to further consolidate their causal relationship.<\/jats:p>\n                  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Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9317-1348","authenticated-orcid":false,"given":"Sarah J.","family":"Glastras","sequence":"additional","affiliation":[{"name":"Department of Diabetes, Endocrinology and Metabolism, Royal North Shore Hospital, St Leonards, New South Wales, Australia"},{"name":"Kolling Institute, Royal North Shore Hospital, St Leonards, New South Wales, Australia"},{"name":"Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia"},{"name":"Australian Centre for Accelerating Diabetes Innovations (ACADI), The University of Melbourne, Parkville, Victoria, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6834-4876","authenticated-orcid":false,"given":"Alexia","family":"Pena","sequence":"additional","affiliation":[{"name":"Discipline of Paediatrics, The University of Adelaide and Robinson 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