Dysregulation of CD36 upon TLR‐2 stimulation in monocytes from patients with atopic dermatitis and the TLR2 R753Q polymorphism

Abstract

The cutaneous colonization with Staphylococcus aureus represents a potent trigger factor of atopic dermatitis. Toll-like receptor (TLR)-2 and CD36 have been shown to play a pivotal role in the internalization of staphylococcal components. To investigate the impact of TLR-2 ligands on cell surface protein expression in monocytes from wild type (WT) AD patients and TLR-2 R753Q polymorph AD patients. CD36 expression was significantly less downregulated in TLR-2 polymorph AD patients compared to wild type AD patients upon stimulation with peptidoglycan (PGN) and lipoteichoic acid (LTA) and compared to healthy controls upon stimulation with PGN. Expression of CD86 was higher upon N-palmitoyl-S-[2,3-bis(palmitoyl)-(2RS)-propyl]-(R)cysteinyl-alanyl-glycine (Pam3Cys) stimulation in TLR-2 R753Q polymorph AD patients compared to wild type AD patients. Expression of CD80 and CD54 were unaffected. The differences in CD36 expression in TLR-2 polymorph AD patients compared to wild type AD patients and healthy controls may be associated with an enhanced susceptibility to skin infections with S. aureus.