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JID Innov. 2021 Aug 23;1(4):100054. doi: 10.1016/j.xjidi.2021.100054. eCollection 2021 Dec.

Deletion of .

JID innovations

Céline Evrard, Emilie Faway, Evelyne De Vuyst, Olivier Svensek, Valérie De Glas, David Bergerat, Michel Salmon, Olivier De Backer, Bruno Flamion, Hélène Le-Buanec, Catherine Lambert de Rouvroit, Yves Poumay

Affiliations

  1. Research Unit of Molecular Physiology (URPhyM), NAmur Research Institute for LIfe Sciences (NARILIS), University of Namur, Namur, Belgium.
  2. Inovarion SAS, Paris, France.
  3. StratiCell, Les Isnes, Belgium.
  4. Laboratory of Oncodermatology, Immunology, and Cutaneous Stem Cells, National Institute of Health and Medical Research (INSERM) U976, Saint-Louis Hospital, Paris, France.

PMID: 34909750 PMCID: PMC8659394 DOI: 10.1016/j.xjidi.2021.100054

Abstract

TSG-6 is a soluble protein secreted in the extracellular matrix by various cell types in response to inflammatory stimuli. TSG-6 interacts with extracellular matrix molecules, particularly hyaluronan (HA), and promotes cutaneous wound closure in mice. Between epidermal cells, the discrete extracellular matrix contains HA and a tiny amount of TSG-6. However, challenges imposed to keratinocytes in reconstructed human epidermis revealed strong induction of TSG-6 expression, after exposure to T helper type 2 cytokines to recapitulate the atopic dermatitis phenotype or after fungal infection that causes secretion of cytokines and antimicrobial peptides. After both types of challenge, enhanced release of TSG-6 happens simultaneously with increased HA production. TSG-6 deficiency in N/TERT keratinocytes was created by inactivating

© 2021 The Authors.

Keywords: AD, atopic dermatitis; ECM, extracellular matrix; GEO, Gene Expression Omnibus; HA, hyaluronan; HAS, hyaluronan synthase; KC, keratinocyte; KLK, kallikrein; RHE, reconstructed human epidermis; RNA-seq, RNA sequencing; Th, T helper type; crRNA, CRISPR RNA

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