Differential efficacy of biologic treatments targeting the TNF-α/IL-23/IL-17 axis in psoriasis and psoriatic arthritis

Furue, Kazuhisa; Ito, Takamichi; Furue, Masutaka

doi:10.1016/j.cyto.2018.08.025

Cited by 69 publications

(69 citation statements)

References 148 publications

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“…Therapeutic strategies for psoriasis are rapidly expanding and maturing because the various biologics targeting the TNF-α/IL-23/IL-17A axis are quite effective and have very satisfactory results, although certain differences exist in the various treatment responses. 46 Notably, biologic treatments improve skin lesions in association with the rapid downregulation of the lesional expression of CCL20 in patients with psoriasis. 25,72 The anti-TNF-α antibody infliximab reduces the lesional expression of CCL20 as early as 16 hours after injection.…”

Section: Target For the Treatment Of Psoriasismentioning

confidence: 99%

“…In addition, the CCL20/CCR6 chemotactic system is critically involved in the maintenance of the TNF‐α/IL‐23/IL‐17A axis. Therapeutic agents for psoriasis include topical steroids, topical vitamin D3 derivatives, phototherapy, phosphodiesterase‐4 inhibitors, cyclosporine, methotrexate and biologics targeting TNF‐α, IL‐23 and IL‐17A . As the TNF‐α/IL‐23/IL‐17A axis plays a pivotal role in the pathogenesis of psoriasis, the efficacy of anti–TNF‐α/IL‐23/IL‐17A biologics is excellent …”

Section: Introductionmentioning

confidence: 99%

“…Therapeutic agents for psoriasis include topical steroids, topical vitamin D3 derivatives, phototherapy, phosphodiesterase-4 inhibitors, cyclosporine, methotrexate and biologics targeting TNF-α, IL-23 and IL-17A. [38][39][40][41][42][43][44][45][46] As the TNF-α/IL-23/IL-17A axis plays a pivotal role in the pathogenesis of psoriasis, the efficacy of anti-TNF-α/IL-23/IL-17A biologics is excellent. 3,24,46 In this review, we will summarize the current research topics regarding the CCL20/CCR6 axis in psoriasis.…”

Section: Introductionmentioning

confidence: 99%

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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: Target For the Treatment Of Psoriasismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The CCL20 and CCR6 axis in psoriasis

et al. 2019

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“…That the tumor necrosis factor-α (TNF-α) and IL-23/IL-17A axes appear to be major drivers in the pathogenesis of psoriasis is underscored by the excellent response of psoriasis to biologics targeting TNF-α, IL-23, and IL-17A, although a difference exists in their efficacy [46][47][48][49][50][51][52][53][54][55][56][57][58][59][60][61]. Anti-TNF-α/IL-23/IL-17A biologics successfully improve psoriatic arthritis [18,56,[62][63][64].…”

Section: Introductionmentioning

confidence: 99%

Interleukin-17A and Keratinocytes in Psoriasis

Furue

Tsuji

et al. 2020

IJMS

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The excellent clinical efficacy of anti-interleukin 17A (IL-17A) biologics on psoriasis indicates a crucial pathogenic role of IL-17A in this autoinflammatory skin disease. IL-17A accelerates the proliferation of epidermal keratinocytes. Keratinocytes produce a myriad of antimicrobial peptides and chemokines, such as CXCL1, CXCL2, CXCL8, and CCL20. Antimicrobial peptides enhance skin inflammation. IL-17A is capable of upregulating the production of these chemokines and antimicrobial peptides in keratinocytes. CXCL1, CXCL2, and CXCL8 recruit neutrophils and CCL20 chemoattracts IL-17A-producing CCR6+ immune cells, which further contributes to forming an IL-17A-rich milieu. This feed-forward pathogenic process results in characteristic histopathological features, such as epidermal hyperproliferation, intraepidermal neutrophilic microabscess, and dermal CCR6+ cell infiltration. In this review, we focus on IL-17A and keratinocyte interaction regarding psoriasis pathogenesis.

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“…Psoriasis is a chronic inflammatory skin disease characterized by thickening and redness of the skin associated with keratinocyte hyperproliferation, skin inflammation with inflammatory cell infiltration in the epidermis and dermis, and (in severe cases) aseptic abscess formation . Cytokines such as IL‐23, IL‐17A, and TNF play important roles for the pathogenesis of the disease, and the Abs against these cytokines are effective in treating the disease . Innate immune responses play important roles in mouse models.…”

Section: Myeloid Clrs In Cutaneous Immunitymentioning

confidence: 99%

Myeloid C-type lectin receptors in skin/mucoepithelial diseases and tumors

Tang

Makusheva

Sun

et al. 2019

Journal of Leukocyte Biology

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Myeloid C‐type lectin receptors (CLRs), which consist of an extracellular carbohydrate recognition domain and intracellular signal transducing motif such as the immunoreceptor tyrosine‐based activation motif (ITAM) or immunoreceptor tyrosine‐based inhibitory motif (ITIM), are innate immune receptors primarily expressed on myeloid lineage cells such as dendritic cells (DCs) and Mϕs. CLRs play important roles in host defense against infection by fungi and bacteria by recognizing specific carbohydrate components of these pathogens. However, these immune receptors also make important contributions to immune homeostasis of mucosa and skin in mammals by recognizing components of microbiota, as well as by recognizing self‐components such as alarmins from dead cells and noncanonical non‐carbohydrate ligands. CLR deficiency not only induces hypersensitivity to infection, but also causes dysregulation of muco‐cutaneous immune homeostasis, resulting in the development of allergy, inflammation, autoimmunity, and tumors. In this review, we introduce recent discoveries regarding the roles of myeloid CLRs in the immune system exposed to the environment, and discuss the roles of these lectin receptors in the development of colitis, asthma, psoriasis, atopic dermatitis, and cancer. Although some CLRs are suggested to be involved in the development of these diseases, the function of CLRs and their ligands still largely remain to be elucidated.

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Differential efficacy of biologic treatments targeting the TNF-α/IL-23/IL-17 axis in psoriasis and psoriatic arthritis

Cited by 69 publications

References 148 publications

The CCL20 and CCR6 axis in psoriasis

The CCL20 and CCR6 axis in psoriasis

Interleukin-17A and Keratinocytes in Psoriasis

Myeloid C-type lectin receptors in skin/mucoepithelial diseases and tumors

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