NOS2 and CCL27: clinical implications for psoriasis and eczema diagnosis and management

Early-onset pediatric atopic dermatitis is characterized by TH2/TH17/TH22-centered inflammation and lipid alterations

“…7 This classifier evaluates levels of inducible nitric oxide synthase (ie, nitric oxide synthase 2 [NOS2]) and CCL27, with increased NOS2 levels characterizing psoriasis and normal or increased CCL27 levels associated with AD. 7,39 Our pediatric samples clearly classified as AD, similar to their adult counterparts (Fig 4, G and H), confirming the clinical AD diagnosis despite the marked differences in the immune phenotype of children compared with adults with AD.…”

Analysis of anti-tumour necrosis factor-induced skin lesions reveals strong T helper 1 activation with some distinct immunological characteristics

“…As anti‐TNF‐induced psoriasiform and spongiotic/eczematous skin lesions were histopathologically consistent with psoriasis and eczema (spongiotic dermatitis), respectively, we assessed these biopsies with an established molecular disease classifier . This classifier consists of the two inflammatory mediators, nitric oxide synthase 2 [NOS2 or inducible nitric oxide synthase (iNOS)] and chemokine (C‐C motif) ligand (CCL) 27, with high NOS2 and low CCL27 mRNA levels being characteristic of psoriasis, and low NOS2 and high CCL27 levels being characteristic of eczema . Surprisingly, neither psoriasiform nor spongiotic/eczematous anti‐TNF‐induced lesions showed a molecular pattern characteristic of classic psoriasis or eczema (Fig.…”

Dissecting susceptibility from exogenous triggers: the model of alopecia areata and associated inflammatory skin diseases

“…In these patients, distinct T‐helper cell subsets induced antagonistic clinical phenotypes in close proximity to each other. The study not only identified mutually exclusive functions of Th1, Th2 and Th17 cells in the skin in vivo and paved the way towards a molecular‐driven individualized medicine in psoriasis and AE, but also served as a proof‐of‐concept study that disease‐specific patterns can be unrevealed by our approach of intra‐individual disease comparison. Investigations whether this approach can be utilized in general to decipher inflammatory phenotypes, however, were still warranted.…”