PuSH - Publikationsserver des Helmholtz Zentrums München

Export: TXT Text RIS Endnote (RIS) BIB BibTeX
Knoop, J. ; Eugster, A.* ; Gavrisan, A. ; Lickert, R. ; Sedlmeier, E.-M. ; Dietz, S.* ; Lindner, A. ; Warncke, K.* ; Hummel, N. ; Ziegler, A.-G. ; Bonifacio, E.

Maternal type 1 diabetes reduces autoantigen-responsive CD4(+) T cells in Offspring.

Diabetes 69, 661-669 (2020)
Verlagsversion Postprint DOI PMC
Open Access Green
Autoimmunity against pancreatic beta -cell autoantigens is a characteristic of childhood type 1 diabetes (T1D). Autoimmunity usually appears in genetically susceptible children with the development of autoantibodies against (pro)insulin in early childhood. The offspring of mothers with T1D are protected from this process. The aim of this study was to determine whether the protection conferred by maternal T1D is associated with improved neonatal tolerance against (pro)insulin. Consistent with improved neonatal tolerance, the offspring of mothers with T1D had reduced cord blood CD4(+) T-cell responses to proinsulin and insulin, a reduction in the inflammatory profile of their proinsulin-responsive CD4(+) T cells, and improved regulation of CD4(+) T cell responses to proinsulin at 9 months of age, as compared with offspring with a father or sibling with T1D. Maternal T1D was also associated with a modest reduction in CpG methylation of the INS gene in cord blood mononuclear cells from offspring with a susceptible INS genotype. Our findings support the concept that a maternal T1D environment improves neonatal immune tolerance against the autoantigen (pro)insulin.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Scopus
Cited By
Altmetric
7.720
1.796
3
6
Tags
Anmerkungen
Besondere Publikation
Auf Hompepage verbergern

Zusatzinfos bearbeiten
Eigene Tags bearbeiten
Privat
Eigene Anmerkung bearbeiten
Privat
Auf Publikationslisten für
Homepage nicht anzeigen
Als besondere Publikation
markieren
Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Immune-responses; Insulin Gene; Human Thymus; Risk; Autoantibodies; Antigen; Autoimmunity; Disease; Children; Birth
Sprache
Veröffentlichungsjahr 2020
HGF-Berichtsjahr 2020
ISSN (print) / ISBN 0012-1797
e-ISSN 1939-327X
Zeitschrift Diabetes
Quellenangaben Band: 69, Heft: 3, Seiten: 661-669 Artikelnummer: , Supplement: ,
Verlag American Diabetes Association
Verlagsort Alexandria, VA.
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Pancreatic Islet Research (IPI)
Institute of Diabetes and Obesity (IDO)
Institute of Diabetes Research (IDF)
POF Topic(s) 90000 - German Center for Diabetes Research
30201 - Metabolic Health
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-502600-006
G-501900-229
G-502100-001
G-501900-217
DOI 10.2337/db19-0751
WOS ID WOS:000530319600017
Scopus ID 85082148232
PubMed ID 31896551
Erfassungsdatum 2020-03-09
[➜Korrektur melden]