Interleukin 36 expression in psoriasis variants and other dermatologic diseases with psoriasis‐like histopathologic features

Abstract

Background: Elevated epidermal interleukin (IL)-36 expression distinguishes psoriasis from eczematous dermatitis, but other psoriasiform dermatitides (PDs) have not been thoroughly investigated for IL-36 expression. In this study, we assess the IL-36 staining pattern (IL36-SP) in psoriasis variants and other PDs including lichen simplex chronicus (LSC), prurigo nodularis (PN), lichen planus (LP), tinea, pityriasis rubra pilaris (PRP), mycosis fungoides (MF), pemphigus foliaceus (PF), acute generalized exanthematous pustulosis (AGEP), impetigo (IMP), and syphilis (SY).Methods: IL-36 immunostaining was performed on 307 cases of psoriasis and various PDs. IL36-SP in the upper epidermis was graded on a scale of 0-4.Results: High IL36-SP occurred in all variants of psoriasis, as well as in AGEP, PRP, PN, tinea, IMP, and LP (P > 0.05). SY, PF, LSC, and MF showed a lower IL36-SP (P ≤ 0.05) compared with psoriasis. Conclusion:All variants of psoriasis exhibit high IL36-SP. IL-36 staining can assist in differentiating MF, PF, SY, and LSC from psoriasis, particularly MF and LSC, which have consistent low IL-36 expression. AGEP, PRP, tinea, IMP, PN, and LP exhibit high IL-36 expression similar to psoriasis, indicating Th17 activation in these diseases.

Utility of IL‐36 immunostaining in distinguishing psoriasis from pityriasis rosea and pityriasis lichenoides

“…6,7,11 In addition to psoriasis, some other inflammatory or infectious skin diseases with a psoriasiform pattern have been shown to highly express IL-36, including pityriasis rubra pilaris, impetigo, prurigo nodularis, dermatophyte infection, and lichen planus, potentially implicating the role of IL-36 and the Th17 pathway in promulgating these diseases. 7 This is in contrast to diseases with a psoriasiform pattern that shows minimal IL-36 expression, including subacute/chronic spongiotic dermatitis, lichen simplex chronicus (LSC), syphilis, pemphigus foliaceus, and MF. 6,7 Based on our findings, PR belongs to the group of skin diseases with a psoriasiform pattern but weak to no expression of IL-36 in the skin, supporting what is reported in the literature regarding its pathophysiology.…”

“…7 This is in contrast to diseases with a psoriasiform pattern that shows minimal IL-36 expression, including subacute/chronic spongiotic dermatitis, lichen simplex chronicus (LSC), syphilis, pemphigus foliaceus, and MF. 6,7 Based on our findings, PR belongs to the group of skin diseases with a psoriasiform pattern but weak to no expression of IL-36 in the skin, supporting what is reported in the literature regarding its pathophysiology. Reactivation of human herpesvirus-6 (HHV-6) and HHV-7 and ingestion of drugs, including angiotensin-converting enzyme inhibitors, may precipitate PR and PR-like eruptions, respectively.…”

“…3,4 Studies conducted in recent years have illustrated high-level expression of IL-36 in psoriatic skin. [5][6][7][8][9][10][11][12] IL-36 immunostaining has been shown to reliably differentiate psoriasis from other inflammatory skin diseases, including various forms of spongiotic dermatitis and other psoriasiform dermatitides. 6,7,11 However, no prior studies have evaluated IL-36 immunostaining in pityriasis rosea (PR), and only one study has assessed the IL-36 immunostaining of five cases of pityriasis lichenoides (PL).…”

“…[5][6][7][8][9][10][11][12] IL-36 immunostaining has been shown to reliably differentiate psoriasis from other inflammatory skin diseases, including various forms of spongiotic dermatitis and other psoriasiform dermatitides. 6,7,11 However, no prior studies have evaluated IL-36 immunostaining in pityriasis rosea (PR), and only one study has assessed the IL-36 immunostaining of five cases of pityriasis lichenoides (PL). 9 In this study, we aim to assess the utility of IL-36 staining to distinguish psoriasis from PR and PL, both of which have overlapping histopathologic features with psoriasis.…”

Kirenol inhibits TNF-α-induced proliferation and migration of HaCaT cells by regulating NF-κB pathway

“…Psoriasis is a recurrent, noninfectious erythema scaly skin disease characterized by epidermal proliferation and inflammation. Its etiology is related to heredity, infection, allergy, metabolic disorders, and autoimmunity (Allergologia et immunopathologia, 2020;Aquino et al, 2021;Evans et al, 2020;Srivastava et al, 2021;Zhou et al, 2020). It is a typical chronic inflammatory disease with an increasing incidence ranging from 1 % to 3 % worldwide (Griffiths & Barker, 2007;Hoegler et al, 2018;Langley et al 2005).…”