Transmembrane protein 232 regulates inflammation in experimental models of atopic dermatitis

Atopic dermatitis (AD) is a prevalent inflammatory skin disorder characterized by dry and itchy skin that may significantly impair a patient’s quality of life.1,2 The ongoing progress of molecular insights into the mechanisms underlying AD has advanced our understanding, revealing important signalling pathways and novel potential targets paving the way for the expanding drug development.3 Interestingly, recent genetic association studies identified TMEM232 to be associated with atopic dermatitis in Asian populations, suggesting it may be implicated in the mechanisms of AD.4–6 Yet, the function of transmembrane protein 232 (TMEM232) has remained unexplored until now. In this issue of the BJD, Han et al. report novel findings using in vitro (human keratinocytes stimulated with different cytokines) and in vivo (mice challenged with MC903) experimental models mimicking AD, demonstrating that TMEM232 may be involved in the dysregulated immune response in AD.7 To explore the role of TMEM232 in regulating inflammation, Tmem232 was knocked down (i.e. reduced gene expression) by short hairpin RNA or overexpressed using a plasmid construct in human keratinocyte cell lines (HaCaT). Interestingly, Tmem232 knockdown markedly decreased proinflammatory cytokine production under tumour necrosis factor/interferon-γ stimulation, whereas Tmem232 overexpression increased proinflammatory cytokine production in unstimulated cells. In line with this, TMEM232 levels were significantly upregulated in the lesional skin of patients with AD compared with healthy donors. These findings provide evidence that TMEM232 may have a significant function in regulating inflammation in AD.