Highlighting Interleukin-36 Signalling in Plaque Psoriasis and Pustular Psoriasis

Furue, Kazuhisa; Yamamura, Ken‐ichi; Tsuji, Gaku; Mitoma, Chikage; Uchi, Hiroshi; Nakahara, Takeshi; Kido‐Nakahara, Makiko; Kadono, Takafumi; Furue, Masutaka

doi:10.2340/00015555-2808

Cited by 96 publications

(119 citation statements)

References 94 publications

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“…Neutrophilic microabscesses are also typical histologic manifestations . Psoriasis has shown a diverse prevalence across populations worldwide: 2.5% in Europeans, 0.05%‐3% in Africans and 0.1%‐0.5% in Asians . Males are twice as likely as females to be affected .…”

Section: Introductionmentioning

confidence: 99%

The CCL20 and CCR6 axis in psoriasis

et al. 2019

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Psoriasis is a TNF‐α/IL‐23/IL‐17A–mediated inflammatory skin disease that causes a significant socioeconomic burden in afflicted patients. IL‐17A–producing immune cells, including Th17 cells, are crucial effector cells in the development of psoriasis. IL‐17A stimulates epidermal keratinocytes to produce CCL20, which eventually recruits CCR6 + Th17 cells into the lesional skin. Thus, the CCL20/CCR6 axis works as a driving force that prepares an IL‐17A–rich cutaneous milieu. In this review, we summarize the current research topics on the CCL20/CCR6 axis and the therapeutic intervention of this axis for psoriasis.

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Section: Introductionmentioning

confidence: 99%

The CCL20 and CCR6 axis in psoriasis

et al. 2019

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“…The inflammatory effect of IL‐36 cytokines is blocked by the naturally occurring IL‐36 antagonist (IL‐36Ra) . The importance of IL‐36 in psoriatic skin inflammation gained greater attention with the discovery that a loss of function in the IL‐36Ra is associated with generalized pustular psoriasis (GPP) psoriasis (generalized pustular psoriasis) . This form of psoriasis has since been renamed as DITRA (deficiency of the interleukin IL‐36 receptor antagonist) .…”

Section: The Concept Of Il‐23–independent Il‐17 Productionmentioning

confidence: 99%

Interleukin‐23 pathway at the enthesis: The emerging story of enthesitis in spondyloarthropathy

Bridgewood

Sharif

Sherlock

et al. 2020

Immunological Reviews

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The inflammatory disorders collectively termed the seronegative spondyloarthropathies (SpA) include ankylosing spondylitis (AS), psoriatic arthritis (PsA), reactive arthritis, the arthritis associated with inflammatory bowel disease including Crohn's disease and ulcerative colitis, the arthritis related to anterior uveitis, and finally, somewhat controversially Behcet's disease. All of these diseases are associated with SNPs in the IL‐23R or the interleukin‐23 (IL‐23) cytokine itself and related downstream signaling JAK pathway genes and the interleukin‐17 (IL‐17) pathway. In rheumatoid arthritis, the target of the immune response is the synovium but the SpA disorders target the tendon, ligament, and joint capsule skeletal anchorage points that are termed entheses. The discovery that IL‐23R–expressing cells were ensconced in healthy murine enthesis, and other extraskeletal anchorage points including the aortic root and the ciliary body of the eye and that systemic overexpression of IL‐23 resulted in a severe experimental SpA, confirmed a fundamentally different immunobiology to rheumatoid arthritis. Recently, IL‐23R–expressing myeloid cells and various innate and adaptive T cells that produce IL‐17 family cytokines have also been described in the human enthesis. Blockade of IL‐23 pathway with either anti‐p40 or anti‐p19 subunits has resulted in some spectacular therapeutic successes in psoriasis and PsA including improvement in enthesitis in the peripheral skeleton but has failed to demonstrate efficacy in AS that is largely a spinal polyenthesitis. Herein, we discuss the known biology of IL‐23 at the human enthesis and highlight the remarkable emerging story of this unique skeletal tissue.

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“…Members of the interleukin (IL)‐36 cytokine family, IL‐36α, IL‐36β, IL‐36γ and IL‐36 receptor antagonist (IL‐36Ra), are recently identified interleukins of the IL‐1 group . The IL‐36 members bind to the same receptor, IL‐36R (previously called IL‐1R‐related protein 2), coupled with the IL‐1 receptor accessory protein (IL1RAP), which is a common subunit shared with IL‐1R and IL‐33R . IL‐36α, IL‐36β and IL‐36γ show similar levels of agonistic activity upon binding to IL‐36R .…”

Section: Introductionmentioning

confidence: 99%

“…Accumulating evidence has indicated the pathogenic role of IL‐36 members in psoriasis and its pustular variant . The mRNA expression of IL‐36α and IL‐36γ is upregulated in the lesional skin of psoriasis in association with increased expression of IL‐17, IL‐23 and tumour necrosis factor‐α .…”

Section: Introductionmentioning

confidence: 99%

“…One of the major biological functions of IL‐36α, IL‐36β and IL‐36γ is their potent neutrophilic and eosinophilic chemoattraction . Therefore, the overexpression of IL‐36s has been documented in various skin diseases such as allergic contact dermatitis, atopic dermatitis, mycosis fungoides, Sézary syndrome, autoimmune blistering diseases, hidradenitis suppurativa and acne .…”

Section: Introductionmentioning

confidence: 99%

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Upregulation of IL‐36 cytokines in folliculitis and eosinophilic pustular folliculitis

et al. 2019

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Background Members of the interleukin (IL)‐36 family, IL‐36α, IL‐36β and IL‐36γ, are potent chemoattractive cytokines for neutrophils and eosinophils. IL‐36 receptor antagonist (IL‐36Ra) inhibits IL‐36α, IL‐36β and IL‐36γ activity. However, the immunohistological expression of IL‐36α, IL‐36β, IL‐36γ and IL‐36Ra has never been addressed in normal follicles, folliculitis or eosinophilic pustular folliculitis (EPF). Methods We performed immunohistochemical staining for IL‐36α, IL‐36β, IL‐36γ and IL‐36Ra using 10 cases of EPF, nine of non‐specific folliculitis, 10 normal skin samples and 10 samples of normal follicles adjacent to a sebaceous naevus as a control. Two dermatologists, who were blind to the patient records, evaluated all of the slides. Results The immunoreactive IL‐36α was hardly detected in the follicular epithelium and epidermis in the normal skin, folliculitis or EPF. The expression of IL‐36β, IL‐36γ and IL‐36Ra was augmented in both folliculitis and EPF compared with that in normal follicles. Negative correlations were detected between IL‐36β and IL‐36Ra and between IL‐36γ and IL‐36Ra in normal follicles; however, these were absent in folliculitis. In contrast to normal follicles and folliculitis, a significant positive correlation between IL‐36β/γ and IL‐36Ra was shown in EPF. Conclusions The overexpression of IL‐36β, IL‐36γ and IL‐36Ra is an integral part of the inflammatory response of folliculitis and EPF. The coordinated expression of IL‐36γ and IL‐36Ra may be related to the pathomechanism of EPF.

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Highlighting Interleukin-36 Signalling in Plaque Psoriasis and Pustular Psoriasis

Cited by 96 publications

References 94 publications

The CCL20 and CCR6 axis in psoriasis

The CCL20 and CCR6 axis in psoriasis

Interleukin‐23 pathway at the enthesis: The emerging story of enthesitis in spondyloarthropathy

Upregulation of IL‐36 cytokines in folliculitis and eosinophilic pustular folliculitis

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