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The population group with which one associates curiosity the most is children. To this day, however, only two caregiver reports have been developed to capture variability in children’s curiosity (Piotrowski et al., 2014; Lee et al., 2023). Both are based on specific theoretical frameworks: the interest-deprivation theory (Litman & Jimerson, 2004) and the violation of expectation framework (e.g., Stahl & Feigenson, 2015). Here, we present a novel measure of general curiosity for children between the ages of 2 and 5 years, in which curiosity is captured more broadly where behavioral expressions were not constrained to any specific theoretical framework. The measure is based on the recently created Infant and Toddler Curiosity Questionnaire (ITCQ; Altmann et al., in prep), currently undergoing validation, which is applicable to infants up to 2 years of age. For the novel Early Child Curiosity Questionnaire (EECQ), we adapted and extended the item list to capture how this slightly older age group may explore their environment to learn about it. The new questionnaire consists of 41 items covering various exploratory behaviors such as “My child pokes at and probes objects to see how they feel (e.g., cotton balls, play dough, tree bark, etc.)” and “My child typically seeks clarification for things they do not understand (e.g., how something works)”. Caregivers are asked to consider the last six months and rate each item on a 7-point Likert scale from 1 (‘strongly disagree’) to 7 (‘strongly agree’) as to how well it reflects their child’s typical behavior. The measure is currently being piloted in the UK, Germany and the Netherlands; thus, we aim to present preliminary results of this international collaboration. The measure will be further developed, and its convergent and discriminant validity evaluated, establishing its internal and external validity for capturing individual differences in curiosity. As a result of this work, the newly developed EECQ will help us better

Bacterial and mitochondrial DNA, sharing an evolutionary origin, act as danger-associated molecular patterns in infectious and sterile inflammation. They both contain immunomodulatory CpG motifs. Interactions between CpG motifs and the complement system are sparsely described, and mechanisms of complement activation by CpG remain unclear. Lepirudin-anticoagulated human whole blood and plasma were incubated with increasing concentrations of three classes of synthetic CpGs: CpG-A, -B, and -C oligodeoxynucleotides and their GpC sequence controls. Complement activation products were analyzed by immunoassays. Cytokine levels were determined via 27-plex beads-based immunoassay, and CpG interactions with individual complement proteins were evaluated using magnetic beads coated with CpG-B. In whole blood and plasma, CpG-B and CpG-C (p < 0.05 for both), but not CpG-A (p > 0.8 for all), led to time- and dose-dependent increase of soluble C5b-9, the alternative complement convertase C3bBbP, and the C3 cleavage product C3bc. GpC-A, -B, and -C changed soluble fluid-phase C5b-9, C3bBbP, and C3bc to the same extent as CpG-A, -B, and -C, indicating a DNA backbone-dependent effect. Dose-dependent CpG-B binding was found to C1q (r = 0.83; p 5 0.006) and factor H (r = 0.93; p < 0.001). The stimulatory complement effect was partly preserved in C2-deficient plasma and completely preserved in MASP-2-deficient serum. CpG-B increased levels of IL-1 beta, IL-2, IL-6, IL-8, MCP-1, and TNF in whole blood, which were completely abolished by inhibition of C5 and C5aR1 (p < 0.05 for all). In conclusion, synthetic analogs of bacterial and mitochondrial DNA activate the complement system via the DNA backbone. We suggest that CpG-B interacts directly with classical and alternative pathway components, resulting in complement-C5aR1-dependent cytokine release.