Few studies have shown a significant increase of CD3(+) T-cell receptor (TC
R) gamma delta in the early phases of type 1 diabetes. We wished to determi
ne if CD3(+) TCR gamma delta is involved in the pathogenesis of gestational
diabetes mellitus (GDM). We studied 29 GDM patients and 21 normal pregnant
women. Lymphocyte subpopulations (CD3(+) TCR ap, CD3(+) TCR gamma delta),
islet cell antibodies (ICA), glutamic acid decarboxylase antibodies (GAD) a
nd protein tyrosine phosphatase antibodies (IA(2)-Ab) were evaluated in all
patients. The percentage of CD3(+) TCR gamma delta was significantly highe
r in GDM women than in the control group (5.1 +/- 2.9% vs 3.7 +/- 1.7%; p <
0.05). No abnormalities of the other lymphocyte subpopulations were found.
All subjects were negative for ICA; 2 GDM patients were positive for GAD,
but no relationship was found between GAD positivity and CD3(+) gamma delta
levels in these 2 patients. Further follow-up studies of these patients ar
e required to verify if the CD3(+) TCR gamma delta receptor is a useful mar
ker for diabetes development.