title: Programmed death-ligand 1, 2 expressions are decreased in the psoriatic epidermis.
abstract: Psoriatic keratinocytes are one of the key components that amplify and maintain chronic inflammation. We hypothesized that lack of proper regulatory functions of keratinocytes can be responsible for chronic inflammation in psoriasis. Programmed death-ligands (PD-L) 1, 2 are expressed on keratinocytes, and expressions by nonlymphoid cells are important for mediating peripheral T cell tolerance. In our study, we investigated whether PD-L1, 2 expressions are altered in keratinocytes of psoriatic epidermis compared to normal epidermis. Epidermis was separated and analyzed for PD-L1, 2 expressions in mRNA and protein levels. Immunohistochemical stainings were done in skin biopsy samples from psoriasis, normal skin, allergic contact dermatitis (ACD), pityriasis rosea (PR) and lichen planus (LP). Expressions of PD-L1, 2 mRNA levels were significantly decreased in psoriatic epidermis compared to normal epidermis. In protein levels, PD-L1 expression was significantly decreased in psoriatic epidermis. However, PD-L2 expression was not detected in both normal and psoriatic epidermis. Immunohistochemical stainings revealed significantly less PD-L1 expression in psoriatic epidermis compared to normal epidermis. Even compared to other cutaneous inflammatory diseases, psoriatic epidermis showed less expression than ACD, PR and LP. PD-L2 expression was minimally detected in normal epidermis and not in psoriatic epidermis, but its expression was increased in ACD, PR and LP. In conclusion, we demonstrated that PD-L1, 2 are decreased in psoriatic epidermis in mRNA and protein levels. In addition, we showed that their expression was significantly lower than other inflammatory skin diseases. We suggest that decreased expression of PD-L1, 2 on psoriatic epidermis can contribute to its chronic unregulated inflammatory characteristics.
authors.affiliation: Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 120-752, Republic of Korea.
authors.forename: Dae Suk
authors.initials: DS
authors.lastname: Kim
authors.forename: Jung Hwan
authors.initials: JH
authors.lastname: Je
authors.forename: Sung Hee
authors.initials: SH
authors.lastname: Kim
authors.forename: Dongyun
authors.initials: D
authors.lastname: Shin
authors.forename: Tae-Gyun
authors.initials: TG
authors.lastname: Kim
authors.forename: Do Young
authors.initials: DY
authors.lastname: Kim
authors.forename: Soo Min
authors.initials: SM
authors.lastname: Kim
authors.forename: Min-Geol
authors.initials: MG
authors.lastname: Lee
mesh_terms: D000293:Adolescent; D000328:Adult; D015153:Blotting, Western; D004817:Epidermis / Q000378:metabolism* / Q000473:pathology; D005260:Female; D015870:Gene Expression / Q000502:physiology / Q000528:radiation effects*; D006801:Humans; D015603:Keratinocytes / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D061027:Programmed Cell Death 1 Ligand 2 Protein / Q000235:genetics / Q000378:metabolism*; D061026:Programmed Cell Death 1 Receptor / Q000235:genetics / Q000378:metabolism*; D011565:Psoriasis / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D055815:Young Adult
chemical_list: C105992:PDCD1 protein, human; C556977:PDCD1LG2 protein, human; D061027:Programmed Cell Death 1 Ligand 2 Protein; D061026:Programmed Cell Death 1 Receptor; D012333:RNA, Messenger