{'fraction_non_alphanumeric': 0.026057401812688823, 'fraction_numerical': 0.005287009063444109, 'mean_word_length': 5.160465116279069, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
In praise of small studies

all volunteers showed such an immunosuppression with sufficiently high UV exposures, a finding more extensively confirmed by the group of Dr Antony Young. Its general occurrence indicates that this immunosuppressive response to UV exposure is likely to be a sound physiological reaction. A lack of such immunosuppression could conceivably lead to illicit immune reactions toward the UV-exposed skin, e.g. directed at neoantigens formed by photochemical reactions. This evokes the image of a ‘sun allergy’, most commonly polymorphic light eruption (PLE). Pursuing this line of reasoning my group found that patients with PLE indeed showed weakened migratory responses of Langerhans cells and CD11b+ ‘macrophage-like’ cells upon UV overexposure; these migratory responses had been linked to the immunosuppression by UV radiation. Subsequently, two groups from the U.K. provided the functional evidence that patients with PLE indeed showed less suppression of contact hypersensitivity after UV exposures around the threshold level for evoking a sunburn [i.e. around 1 minimal erythema dose (MED)]. In these earlier studies the lack of immunosuppression was established with UV doses matched to an individual’s sunburn sensitivity, i.e. doses in MEDs. Interestingly, the MEDs tended to be somewhat lower in patients with PLE than in controls, and Koulu et al. found that when patients with PLE and healthy controls were exposed to the same absolute level of UV radiation (4 standard erythema doses) there was no apparent difference in immunosuppression between the two groups. There was, however, a significantly lower percentage of patients with PLE in whom allergen-specific tolerance was induced. This lack of tolerance could be related to a lower influx of (CD11b+) neutrophils in patients with PLE which is normalized after a course of UV hardening, which also results in a slight increase in MED (by approximately 40%). In the paper by Gruber-Wackernagel et al. in this issue, the known immunosuppressive effect of a noncalcaemic 1,25dihydroxyvitamin D3 analogue is successfully tested on artificial provocation of PLE, i.e. repeated prior topical application of calcipotriol lessened PLE responses to successive daily UV exposures. Remarkably, the calcipotriol treatment also resulted in a slight increase in MED (by approximately 40%). Considering that our vitamin D status is largely determined by solar UV exposure, the question emerges to what extent the susceptibility to PLE is enhanced by low vitamin D levels after a winter, and to what extent UV hardening could be attributable to increased vitamin D levels.