Nonlesional atopic dermatitis skin shares similar T‐cell clones with lesional tissues

Abstract

While AD harbors a highly polyclonal T-cell receptor repertoire, and despite the lack of information on TCR antigen specificity, the sharing of top abundant clones between lesional and nonlesional skin, and their persistence after months of therapy, points to the continuous presence of potentially pathogenic skin resident memory T cells well beyond clinically inflamed lesions.

Dupilumab progressively improves systemic and cutaneous abnormalities in patients with atopic dermatitis

“…Circulating type 2 chemokines have been implicated as biomarkers of AD severity at baseline or as markers of treatment response, and they include CCL17, CCL18, ECP, and periostin. 11,89,[153][154][155][156][157][158] CCL17 and CCL18 are chemokines that attract and activate inflammatory cells expressing CCR4 and CCR8 receptors, whereas the extracellular matrix protein periostin amplifies keratinocyte responses. In our study dupilumab significantly suppressed serum levels of all of these biomarkers, as well as total and allergen-specific IgE concentrations.…”

Langerhans and inflammatory dendritic epidermal cells in atopic dermatitis are tolerized toward TLR2 activation

“…It is assumed that TLR2 plays a crucial role in the recognition and defense toward S. aureus . Cutaneous TLR2 activation was reported to suppress T‐cell immune responses . In impetiginized skin from patients with AD, a biologically active amount of TLR2 ligand lipoteichoic acid was detected .…”

Clonotypic Heterogeneity In Cutaneous T-Cell Lymphoma Revealed By Comprehensive Whole Exome/Transcriptome Sequencing

“…pseudogenes TRAV11, TRAV28, TRAV31, TRBV12-1, TRBV22-1). 27,28 We hypothesize that the putative increased frequency of pathogen recognizing Vβ usage may be due to presence of reactive Tcell in the sample, which was minimized in our material which was microdissected and enriched in neoplastic cells.…”