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who reported elevated levels in all anti-��2GP1-IgG subclasses, even including IgG4, in patients with APS compared to a control group of healthy adults [23]. It might be that the elevated absolute OD values of the anti-��2GP1-IgG subclasses are the logical consequence of the generally higher level of anti-��2GP1-IgG in the patients with APS and healthy Selleckchem Ku0059436 children who were selected for further testing. Therefore, we also analysed the subclass distribution of this antibody. We first analysed the anti-��2GP1-IgG subclass distribution within the individual cohorts and observed that in the healthy children the IgG3 antibody was most abundant with a contribution of 40% to the total reactivity. This is consistent with the finding that all sera of the healthy children were seropositive in this subclass and that their anti-��2GP1-IgG3 OD values were the highest of all cohorts. This indicates a predominance of this subclass in the healthy children. The remaining anti-��2GP1-IgG subclasses in the sera of the children ranged from 15% (IgG1) over 20% (IgG2) to 25% (IgG4) but the differences between their proportions were not statistically significant. In contrast, in the sera of the patients with APS, the anti-��2GP1-IgG2 subclass had the highest contribution with 38%. The finding of an elevated proportion of the IgG2 subclass in the patients with APS confirms former published data which also describe a skewing towards anti-��2GP1-IgG2 in APS [19, 23, 26, 27]. The authors detected an even higher contribution of anti-��2GP1-IgG2 (70.2% [26] and 87% [27], resp.). In contrast to our results, the IgG1 subclass was more prominent in the published studies described above. Importantly, in the cohort of the healthy infants IgG2 was relatively low. Therefore one may argue that anti-��2GP1-IgG2 is not just a marker of the disease but is also involved in the pathogenic action of the aPL autoantibodies. When we compared the anti-��2GP1-IgG subclass distribution between the three cohorts, we noticed a significant difference in the distribution concerning the children on one hand and NHD and patients with APS on the other. Healthy children showed a higher proportion of anti-��2GP1-IgG3 and a lower one of anti-��2GP1-IgG2. In NHD and patients with APS, it was the other way round. IgG1 and IgG4 did not significantly differ between healthy children and patients with APS or NHD. The predominance of anti-��2GP1-IgG3 in the healthy children is a hint to an immune response elicited by a proteinaceous antigen [26, 27, 34]. This supports the hypothesis that the harmless anti-��2GP1 in children are infection-induced with pathogen-derived proteins serving as trigger for their production. However, it is still elusive if the IgG3-dominated anti-��2GP1 response, found in the sera of healthy children, contributes to its low pathogenic potential.