Background: The immunogenetic predisposition
may be considered as an important factor for the
development of Type 1 Diabetes Mellitus (T1DM)
in association with the HLA antigens.
Objective:This study was designed to investigate
the role of HLA-class II antigens in the etiology of
type T1DM and in prediction of this disease in
siblings, and its effect on expression of glutamic
acid decarboxylase autoantibodies (GADA).
methods:Sixty children who were newly diagnosed
type 1 diabetes (diagnosed less than five months)
were selected. Their age ranged from 3-17 years.
Another 50 healthy siblings were available for this
study, their ages range from 3-16 years. Eighty
apparently healthy control subjects, matched with
age (4-17) years, sex and ethnic backgrounds
(Iraqi Arabs) underwent the HLA-typing
examination. Finally 50 healthy individuals were
selected randomly to undergo GADA test.
Results:At HLA-class II region, DR3 and DR4
were significantly increased in patients (53.33
vs.26.25% and 50.0 vs. 12.5% respectively) as
compared to controls. In
addition to that, T1DM was significantly associated
with DQ2 (33.33 vs.15%) and DQ3 (40.0 vs.20%)
antigens as compared to controls, suggesting that
these antigens had a role in disease susceptibility,
while the frequency of DR2 and DQ1 antigens were
significantly lowered in patients compared to
controls (6.66 vs.25% and 6.66 vs.22.5%
respectively). These molecules might have
protective effect. In siblings a significant increase
frequency of DR4 antigen (34.0 vs.12.5%) was
observed in comparison to controls, suggesting that
it might be much useful for predicting T1DM in
affected families.Anti-GAD autoantibodies were
present in 50% of Type 1Diabetic children, and in
16% of their siblings. High proportion of GADA
was found in the patients carrying HLA-DR3/DR4
heterozygous.
conclusion:Both the T1DM patients and their
siblings shared the HLA- DQ1 as protective
antigens, while DR3 and DR4 were susceptible one,
and high proportion of GADA was found in the
T1DM patients and siblings carrying HLADR3/DR4 heterozygous
Abstract
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