{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,28]],"date-time":"2026-07-28T00:25:35Z","timestamp":1785198335834,"version":"3.55.0"},"reference-count":12,"publisher":"American Diabetes Association","issue":"7","license":[{"start":{"date-parts":[[2021,8,27]],"date-time":"2021-08-27T00:00:00Z","timestamp":1630022400000},"content-version":"vor","delay-in-days":4153,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/3.0\/"}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2010,7,1]]},"abstract":"<jats:sec>\n                  <jats:title>OBJECTIVE<\/jats:title>\n                  <jats:p>Monocytes in childhood-onset type 1 diabetes show distinct gene expression. We hypothesize that monocyte activation in monozygotic (MZ) twin pairs discordant for childhood-onset type 1 diabetes could reflect distinct stages of the disease process including diabetes susceptibility (differences between twins, both diabetic and nondiabetic, and control subjects) and\/or disease progression (differences between diabetic and nondiabetic twins).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESEARCH DESIGN AND METHODS<\/jats:title>\n                  <jats:p>We studied patterns of inflammatory gene expression in peripheral blood monocytes of MZ twin pairs (n = 10 pairs) discordant for childhood-onset type 1 diabetes, normal control twin pairs (n = 10 pairs), and healthy control subjects (n = 51) using quantitative-PCR (Q-PCR). We tested the 24 genes previously observed by whole genome analyses and verified by Q-PCR in autoimmune diabetes and performed a hierarchical cluster analysis.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESULTS<\/jats:title>\n                  <jats:p>Of 24 genes abnormally expressed in childhood-onset type 1 diabetes, we revalidated abnormal expression in 16 of them in diabetic twins including distinct sets of downregulated (P &amp;lt; 0.03) and upregulated (P &amp;lt; 0.02) genes. Of these 16 genes, 13 were abnormally expressed in nondiabetic twins, implicating these genes in diabetes susceptibility (P &amp;lt; 0.044 for all). Cluster analysis of monocyte gene-expression in nondiabetic twins identified two distinct, mutually exclusive clusters, while diabetic twins had a network of positively correlated genes.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>CONCLUSIONS<\/jats:title>\n                  <jats:p>Patients with childhood-onset type 1 diabetes show abnormal monocyte gene\u2013expression levels with an altered gene\u2013expression network due to gene-environment interaction. Importantly, perturbed gene\u2013expression clusters were also detected in nondiabetic twins, implicating monocyte abnormalities in susceptibility to diabetes.<\/jats:p>\n               <\/jats:sec>","DOI":"10.2337\/db09-1433","type":"journal-article","created":{"date-parts":[[2010,4,15]],"date-time":"2010-04-15T02:21:38Z","timestamp":1271298098000},"page":"1751-1755","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":34,"title":["Monocyte Gene-Expression Profiles Associated With Childhood-Onset Type 1 Diabetes and Disease Risk: A Study of Identical Twins"],"prefix":"10.2337","volume":"59","author":[{"given":"Huriya","family":"Beyan","sequence":"first","affiliation":[{"name":"Blizard Institute of Cell and Molecular Science, Queen Mary, University of London, London, U.K.;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roosmarijn C.","family":"Drexhage","sequence":"additional","affiliation":[{"name":"Department of Immunology, Erasmus Medical Center, Rotterdam, the Netherlands;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leonie","family":"van der Heul Nieuwenhuijsen","sequence":"additional","affiliation":[{"name":"Department of Immunology, Erasmus Medical Center, Rotterdam, the Netherlands;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harm","family":"de Wit","sequence":"additional","affiliation":[{"name":"Department of Immunology, Erasmus Medical Center, Rotterdam, the Netherlands;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roosmarijn C.","family":"Padmos","sequence":"additional","affiliation":[{"name":"Department of Immunology, Erasmus Medical Center, Rotterdam, the Netherlands;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nanette C.","family":"Schloot","sequence":"additional","affiliation":[{"name":"Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University D\u00fcsseldorf and the Department of Medicine\/Metabolic Diseases, University Hospital, D\u00fcsseldorf, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hemmo A.","family":"Drexhage","sequence":"additional","affiliation":[{"name":"Department of Immunology, Erasmus Medical Center, Rotterdam, the Netherlands;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard David","family":"Leslie","sequence":"additional","affiliation":[{"name":"Blizard Institute of Cell and Molecular Science, Queen Mary, University of London, London, U.K.;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1167","published-online":{"date-parts":[[2010,4,14]]},"reference":[{"key":"2022031208590421400_B1","doi-asserted-by":"crossref","first-page":"221","DOI":"10.1016\/S0140-6736(01)05415-0","article-title":"Type 1 diabetes: new perspectives on disease 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