Skip to main content
Fig. 1 | Biomedical Dermatology

Fig. 1

From: Toll-like receptor 2 plays a critical role in pathogenesis of acne vulgaris

Fig. 1

TLR-mediated inflammatory cytokine induction. P. acnes secreted lipases, proteases, and hyaluronidases which can be recognized by TLR2 of keratinocytes nearby sebaceous follicles primarily. Next, the invading signals are transported from ECD dimerization of TLR2 and TLR1/6 to TIR dimerization of TLR2 and TLR1/6. TIR dimerization recruits adaptor proteins including MAL and MyD88. Adaptor proteins initiate phosphorylation of IRAK and promote TRAF6 activation that facilitates the phosphorylation of IKK and release of IκB. NF-κB translocates to the nucleus after disassociation with IκB and transcribes cytokines. As a result, cytokines induce inflammatory acne in the sebum-clogged pore and lasting cytokine levels may contribute to progress acute acne into chronic disease

Back to article page