Advances in atopic dermatitis and urticarial in 2016 Tetsuya Honda, MD, PhD, Takashi Nomura, MD, PhD, Kenji Kabashima, MD, PhD  Journal of Allergy and Clinical Immunology  Volume 140, Issue 2, Pages 369-376 (August 2017) DOI: 10.1016/j.jaci.2017.06.005 Copyright © 2017 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 1 A graphic summary of key advances in the pathogenesis and treatment in patients with AD. A, Dupilumab blocks signaling from IL-4 and IL-13 and inhibits TH2-type inflammation. Nemolizumab blocks signaling from IL-31 and suppresses itch. One of the mechanisms might be through inhibition of nerve elongation and branching. B, Lack of filaggrin leads to enhanced LC activation, which might cause reduced Treg cell numbers in the skin. C, Pediatric AD shows higher induction of TH17-related cytokines than adult AD. peTH2 cells might play crucial roles in the development of AD. D, Regulatory mechanisms of S aureus colonization in the skin. AMPs from IL-22–activated keratinocytes or from coagulase-negative Staphylococcus species (CoNS) restrict the spread of Staphylococcus aureus. S aureus escapes from adaptive immunity by inducing T-cell paralysis through lipoteichoic acid (LTA). E, Dysbiosis in the gut (increase of Faecalibacterium prausnitzii) leads to decreased levels of anti-inflammatory short-chain fatty acids, such as butyrate and propionate, which can cause an impaired epithelial barrier and aggravate TH2-type immune responses in the skin. Journal of Allergy and Clinical Immunology 2017 140, 369-376DOI: (10.1016/j.jaci.2017.06.005) Copyright © 2017 American Academy of Allergy, Asthma & Immunology Terms and Conditions