SummaryAtopic dermatitis (AD) is the most common allergic inflammatory skin disease. Interactions of genetic, environmental and immunological factors result in the initiation and progress of AD. Although the clinical picture, characterized by acute flare-ups of eczematous, pruritic lesions on dry skin at typical predilection such as the flexural folds, is quite homogenous, the trigger factors of the disease are diverse and the pathophysiologic network involved is complex. Therefore, first attempts have been made to classify subtypes of AD based on the most relevant causal factors in the individual patient. To optimize such a stratification of patients, detailed knowledge about cofactors impacting on manifestation of AD as well as impairment of the course of the disease is indispensable. AD shares general features of barrier dysfunction and skin inflammation with other inflammatory diseases of the skin such as psoriasis or allergic contact dermatitis, but a plethora of disease-specific genetic, immunologic and environmental factors have been identified in AD as well. It is the purpose of this review to illustrate key concepts of the pathogenesis of AD. Important findings of recent years will be summarized and cofactors of the pathogenesis will be controversially discussed. We will summarize knowledge on pathogenic factors on the immunologic level contributing to skin barrier dysfunction in AD and the role of the microbiome as first line of defence. Furthermore, we will elucidate the role of innate lymphoid cells in AD and outline the pattern of T helper cell subtypes present in the skin during different stages of AD.

In view of our data, different mucosal regions such as the vestibulum might represent alternative SLIT application sites with potent allergen uptake. Our data might serve as a basis for new application strategies for SLIT to enhance efficiency and reduce local adverse reactions.

No abstract

These observations suggest that the TLR9 promoter polymorphism C-1237T might affect AE susceptibility in particular in patients with the intrinsic variant of AE.

The pandemic condition Coronavirus‐disease (COVID‐19), caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) can take asymptomatic, mild, moderate, and severe courses. COVID‐19 affects primarily the respiratory airways leading to dry cough, fever, myalgia, headache, fatigue, and diarrhea and can end up in interstitial pneumonia and severe respiratory failure. Reports about the manifestation of various skin lesions and lesions of the vascular system in some subgroups of SARS‐CoV‐2 positive patients as such features outside the respiratory sphere, are rapidly emerging. Vesicular, urticarial and maculopapular eruptions as well as livedo, necrosis and other vasculitis forms have been reported most frequently in association with SARS‐CoV‐2 infection. In order to update information gained, we provide a systematic overview of the skin lesions described in COVID‐19 patients, discuss potential causative factors and describe differential diagnostic evaluations. Moreover, we summarize current knowledge about immunologic, clinical and histologic features of virus‐ as well as drug‐induced lesions of the skin and changes to the vascular system in order to transfer this knowledge to potential mechanisms induced by SARS‐CoV‐2.