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Füchtenbusch, M.* ; Bonifacio, E.* ; Lampasona, V.* ; Knopff, A.* ; Ziegler, A.-G.*

Immune responses to glutamic acid decarboxylase and insulin in patients with gestational diabetes.

Clin. Exp. Immunol. 135, 318-321 (2004)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Pregnancy is a natural state of immunoprotection and tolerance. We studied subjects with gestational diabetes (GDM) to evaluate the influence of pregnancy on the humoral immune response to the autoantigen GAD and to injected insulin. Antibodies against glutamic acid decarboxylase (GADA) subclasses and epitope reactivity were determined in 34 GADA-positive pregnant patients with GDM, in 20 GADA-positive relatives of people with TID and in 25 GADA-positive patients with newly diagnosed TID. Partum levels of insulin antibodies (IA), IgG1- and IgG4-IA were measured in 131 women with GDM treated with human insulin from the time of diabetes diagnosis (including 22 with GADA) and were compared to 19 patients with TID after 3 months of insulin treatment. GADA titre and subclasses were similar among all groups. GADA in GDM patients bound fewer epitopes than GADA in relatives of patients with TID (all epitopes being present in 23%versus 65%, P < 0.01). In particular, antibodies to the minor GADA epitopes GAD6596-249, GAD651-100 and GAD67 were less frequent in patients with GDM compared to relatives (P < 0.01). Antibodies to insulin (IA) were found in 17% of patients with GDM. They were more frequent in GDM patients with GADA compared to GADA-negative patients (41%versus 12%, P < 0.005). IgG1 was the dominant insulin antibody subclass response in both patients with GDM and TID but levels of IgG1-IA and IgG4-IA were significantly lower in patients with GDM compared to patients with TID (P < 0.004). Antibody responses in women with gestational diabetes appear to be dampened and restricted, but without change in subclass usage.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Sprache englisch
Veröffentlichungsjahr 2004
HGF-Berichtsjahr 0
ISSN (print) / ISBN 0009-9104
e-ISSN 1365-2249
Quellenangaben Band: 135, Heft: 2, Seiten: 318-321 Artikelnummer: , Supplement: ,
Verlag Wiley
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)
Institute of Diabetes Research (IDF)
Institute of Pancreatic Islet Research (IPI)
POF Topic(s) 30502 - Diabetes: Pathophysiology, Prevention and Therapy
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-502290-001
PubMed ID 14738462
Erfassungsdatum 2004-02-00