Timothy Hinks

@HinksLab

The Hinks Lab investigate the immunopathogenesis of airway diseases and pulmonary infections.

University of Oxford, England

Joined November 2017

98 Following

417 Followers

142 Posts

HinksLab retweeted

Allergy EAACI

@AllergyEaaci

4 months ago

The #skin, as the body's largest immune organ, functions as a critical #barrier between host tissues and the external environment. #Disruption of this interface - whether by environmental pollutants, pathogens, or physical damage - triggers alarmin release and downstream activation of type 2 immune responses. In atopic dermatitis, barrier dysfunction is compounded by cutaneous microbial dysbiosis, characterized by reduced microbial diversity and Staphylococcus aureus dominance. This dysbiotic state drives local recruitment of T cells, dendritic cells, and macrophages, perpetuating a self-reinforcing cycle of inflammation, pruritus, and progressive barrier degradation. In this issue, Czarnowicki et al. comprehensively review the mechanisms and clinical implications in atopic dermatitis and psoriasis, contrasting their divergent immune pathways. Yamamura and Dahabreh et al. investigate OX40/OX40L axis in promoting Th2 effector activity and impairing regulatory T cell function in atopic dermatitis. Skoog and Yang et al. integrate methylome, transcriptome, and microbiome analyses in atopic dermatitis, revealing widespread epigenomic remodeling and identifying Rho GTPase-linked immune-epithelial crosstalk. Gluud et al. demonstrate that Staphylococcus aureus superantigens augment epithelial skin barrier damage in cutaneous T cell lymphoma through T cell-driven, JAK-dependent downregulation of structural barrier proteins, identifying a vicious cycle with potential relevance to other inflammatory skin diseases including atopic dermatitis. Yamamura et al. investigate lipid mediators that modulate cytokine production involved in Th skewing in atopic dermatitis. Preis et al. identify reduced cord blood regulatory B10 cells as an early immune predictor of atopic dermatitis. Li et al. demonstrate that short-term sodium dodecyl sulfate exposure causes skin barrier disruption with distinct molecular signatures, and that antioxidants N-acetylcysteine and nicotinamide effectively mitigate surfactant-induced damage and accelerate barrier recovery. Fukushima-Nomura and Kawasaki et al. present IL-22 and IL-18 as potential longitudinal blood biomarkers for monitoring disease activity in dupilumab-treated atopic dermatitis. Ni and Nanan report that despite similar clinical outcomes, White and Asian patients with atopic dermatitis show distinct baseline immune signaling profiles. Suhrkamp, Heidland and Saft et al. show a functional specific IgE and Th2 response toward Malassezia spp. in atopic dermatitis with head and neck dermatitis. Thormann and Arms et al. retrospectively characterize adverse reactions in patients with atopic dermatitis patients treated with biologics and JAK inhibitors, classifying them according to underlying immunologic mechanisms. Gómez-Olarte et al. investigate the link between maternal polyphenol markers in late pregnancy and the lifetime prevalence of atopic dermatitis, food sensitization, wheezing, and bronchitis. Hayashi et al. analyze fecal microbiota composition and lipid mediator profiles in dogs with concurrent canine atopic dermatitis and adverse food reaction. Tsuang et al. use electrical impedance spectroscopy to show that impaired neonatal skin barrier function is associated with atopic dermatitis development in the first year of life in infants at high risk for allergic disease. Bieber and Lauffer discuss the concept of therapeutic speed in atopic dermatitis, contrasting fast-acting agents such as JAK inhibitors with slower, potentially disease-modifying therapies targeting the OX40-OX40L axis.

Timothy Hinks

@HinksLab

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