@article{KaderAzeemJwayedetal.2021,
  author    = {Kader, Hidaya A. and Azeem, Muhammad and Jwayed, Suhib A. and Al-Shehhi, Aaesha and Tabassum, Attia and Ayoub, Mohammed Akli and Hetta, Helal F. and Waheed, Yasir and Iratni, Rabah and Al-Dhaheri, Ahmed and Muhammad, Khalid},
  title     = {Current insights into immunology and novel therapeutics of atopic dermatitis},
  series = {Cells},
  volume    = {10},
  journal   = {Cells},
  number    = {6},
  issn      = {2073-4409},
  doi       = {10.3390/cells10061392},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-241008},
  year      = {2021},
  abstract  = {Atopic dermatitis (AD) is one of the most prevalent inflammatory disease among non-fatal skin diseases, affecting up to one fifth of the population in developed countries. AD is characterized by recurrent pruritic and localized eczema with seasonal fluctuations. AD initializes the phenomenon of atopic march, during which infant AD patients are predisposed to progressive secondary allergies such as allergic rhinitis, asthma, and food allergies. The pathophysiology of AD is complex; onset of the disease is caused by several factors, including strong genetic predisposition, disrupted epidermal barrier, and immune dysregulation. AD was initially characterized by defects in the innate immune system and a vigorous skewed adaptive Th2 response to environmental agents; there are compelling evidences that the disorder involves multiple immune pathways. Symptomatic palliative treatment is the only strategy to manage the disease and restore skin integrity. Researchers are trying to more precisely define the contribution of different AD genotypes and elucidate the role of various immune axes. In this review, we have summarized the current knowledge about the roles of innate and adaptive immune responsive cells in AD. In addition, current and novel treatment strategies for the management of AD are comprehensively described, including some ongoing clinical trials and promising therapeutic agents. This information will provide an asset towards identifying personalized targets for better therapeutic outcomes.},
  language  = {en}
}
@article{FuhrmannTeschRomanosetal.2020,
  author    = {Fuhrmann, Saskia and Tesch, Falko and Romanos, Marcel and Abraham, Susanne and Schmitt, Jochen},
  title     = {ADHD in school-age children is related to infant exposure to systemic H1-antihistamines},
  series = {Allergy},
  volume    = {75},
  journal   = {Allergy},
  number    = {11},
  doi       = {10.1111/all.14411},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-215982},
  pages     = {2956 -- 2957},
  year      = {2020},
  language  = {en}
}
@article{RossbergKellerIckeetal.2020,
  author    = {Roßberg, Siri and Keller, Theresa and Icke, Katja and Siedmann, Valentina and Lau, Imke and Keil, Thomas and Lau, Susanne},
  title     = {Orally applied bacterial lysate in infants at risk for atopy does not prevent atopic dermatitis, allergic rhinitis, asthma or allergic sensitization at school age: Follow-up of a randomized trial},
  series = {Allergy},
  volume    = {75},
  journal   = {Allergy},
  number    = {8},
  doi       = {10.1111/all.14247},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-213456},
  pages     = {2020 -- 2025},
  year      = {2020},
  abstract  = {Background The allergy preventive effects of gut immune modulation by bacterial compounds are still not fully understood. Objective We sought to evaluate the effect of bacterial lysate applied orally from the second until seventh months of life on the prevalence of allergic diseases at school age. Methods In a randomized, placebo-controlled trial, 606 newborns with at least one allergic parent received orally a bacterial lysate consisting of heat-killed Gram-negative Escherichia coli Symbio and Gram-positive Enterococcus faecalis Symbio or placebo from week 5 until the end of month 7. A total of 402 children were followed until school age (6-11 years) for the assessment of current atopic dermatitis (AD), allergic rhinitis (AR), asthma and sensitization against aeroallergens. Results AD was diagnosed in 11.0\% (22/200) of children in the active and in 10.4\% (21/202) of children in the placebo group. AR was diagnosed in 35\% (70/200) of children in the active and in 38.1\% (77/202) children in the placebo group. Asthma was diagnosed in 9\% (18/199) of children in the active and in 6.6\% (13/197) of children in the placebo group. Sensitization occurred in 46.5\% (66/142) of participants in the active and 51.7\% (76/147) in the placebo group. Conclusion An oral bacterial lysate of heat-killed Gram-negative Escherichia coli and Gram-positive Enterococcus faecalis applied during the first 7 months of life did not influence the development of AD, asthma and AR at school age.},
  language  = {en}
}
@article{ZadehKhorasaniNolteMuelleretal.2013,
  author    = {Zadeh-Khorasani, Maryam and Nolte, Thomas and Mueller, Thomas D. and Pechlivanis, Markos and Rueff, Franziska and Wollenberg, Andreas and Fricker, Gert and Wolf, Eckhard and Siebeck, Matthias and Gropp, Roswitha},
  title     = {NOD-scid IL2R \(\gamma^{null}\) mice engrafted with human peripheral blood mononuclear cells as a model to test therapeutics targeting human signaling pathways},
  series = {Journal of Translational Medicine},
  volume    = {11},
  journal   = {Journal of Translational Medicine},
  number    = {4},
  issn      = {1479-5876},
  doi       = {10.1186/1479-5876-11-4},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-122960},
  year      = {2013},
  abstract  = {Background: Animal models of human inflammatory diseases have limited predictive quality for human clinical trials for various reasons including species specific activation mechanisms and the immunological background of the animals which markedly differs from the genetically heterogeneous and often aged patient population. Objective: Development of an animal model allowing for testing therapeutics targeting pathways involved in the development of Atopic Dermatitis (AD) with better translatability to the patient. Methods: NOD-scid IL2R \(\gamma^{null}\) mice engrafted with human peripheral blood mononuclear cells (hPBMC) derived from patients suffering from AD and healthy volunteers were treated with IL-4 and the antagonistic IL-4 variant R121/Y124D (Pitrakinra). Levels of human (h) IgE, amount of B-, T- and plasma-cells and ratio of CD4 : CD8 positive cells served as read out for induction and inhibition of cell proliferation and hIgE secretion. Results were compared to in vitro analysis. Results: hIgE secretion was induced by IL-4 and inhibited by the IL-4 antagonist Pitrakinra in vivo when formulated with methylcellulose. B-cells proliferated in response to IL-4 in vivo; the effect was abrogated by Pitrakinra. IL-4 shifted CD4 : CD8 ratios in vitro and in vivo when hPBMC derived from healthy volunteers were used. Pitrakinra reversed the effect. Human PBMC derived from patients with AD remained inert and engrafted mice reflected the individual responses observed in vitro. Conclusion: NOD-scid IL2R \(\gamma^{null}\) mice engrafted with human PBMC reflect the immunological history of the donors and provide a complementary tool to in vitro studies. Thus, studies in this model might provide data with better translatability from bench to bedside.},
  language  = {en}
}