Interleukin-25 is involved in cutaneous T-cell lymphoma progression by establishing a T helper 2-dominant microenvironment

Nakajima, Rina; Miyagaki, Tomomitsu; Hirakawa, Masahiro; Oka, Tomonori; Takahashi, Naomi; Suga, Hiraku; Yoshizaki, Ayumi; Fujita, Hideki; Asano, Yoshihide; Sugaya, Makoto; Sato, Shinichi

doi:10.1111/bjd.16237

Cited by 20 publications

(24 citation statements)

References 40 publications

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“…In regard to T cell polarization, despite the heterogeneity in expression and varying coexpression levels of Tbet, GATA3, FoxP3, and Bcl6, malignant T cells showed a Th2-predominant phenotype, as it has been previously described ( Supplementary Fig. 5a, b) 13,14 . When broken down by molecular subtype, signature B samples exhibited significantly higher GATA3 and lower Tbet expression ( Fig.…”

supporting

confidence: 64%

Targeted genomic analysis of cutaneous T cell lymphomas identifies a subset with aggressive clinicopathological features

et al. 2020

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supporting

confidence: 64%

Targeted genomic analysis of cutaneous T cell lymphomas identifies a subset with aggressive clinicopathological features

et al. 2020

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“…Additionally, IL-25 is highly expressed in CTCL and promotes the production of Th2 cytokines, in particular IL-13, and eosinophil infiltration. Moreover, TSLP activates dendritic cells to induce Th2-mediated inflammation, and periostin induces chronic inflammation by stimulating TSLP production in CTCL [104,106,107]. This polarized Th2 cytokine pattern is less prominent in the early stages of MF, when Th1-derived IFN-γ is frequently detected, and emerges more markedly with time, as the Th2-bias of malignant T cells [106,107].…”

Section: Mycosis Fungoides and Sézary Syndromementioning

confidence: 99%

Pruritus as a Distinctive Feature of Type 2 Inflammation

et al. 2021

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Pruritus is a common symptom of several skin diseases, both inflammatory and neoplastic. Pruritus might have a tremendous impact on patients’ quality of life and strongly interfere with sleep, social, and work activities. We review the role of type-2 inflammation and immunity in the pathogenesis of chronic pruritic conditions of the skin. Type 2 cytokines, including IL-4, IL-13, thymic stromal lymphopoietin, periostin, IL-31, IL-25, and IL-33 are released by mast cells, innate lymphoid cells 2, keratinocytes, and type 2 T lymphocytes, and are master regulators of chronic itch. These cytokines might act as direct pruritogen on primary sensory neurons (pruriceptors) or alter the sensitivity to other itch mediators Type 2 inflammation- and immunity-dominated skin diseases, including atopic dermatitis, prurigo nodularis, bullous pemphigoid, scabies, parasitic diseases, urticaria, and Sézary syndrome are indeed conditions associated with most severe pruritus. In contrast, in other skin diseases, such as scleroderma, lupus erythematosus, hidradenitis suppurativa, and acne, type 2 inflammation is less represented, and pruritus is milder or variable. Th2 inflammation and immunity evolved to protect against parasites, and thus, the scratching response evoked by pruritus might have developed to alert about the presence and to remove parasites from the skin surface.

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“…Periostin, IL-4 and IL-13 have in addition been reported to stimulate primary human keratinocytes to express increased levels of the cytokine IL-25, which promotes Th2 immunity and cytokine production (Xu and Dong, 2017;Nakajima et al, 2018). Accordingly, the expression of IL-25 is increased in the epidermal keratinocytes in advanced CTCL skin lesions and enhances the expression of IL-13 in IL-25 receptor-positive malignant T cells via activation of STAT6 (Nakajima et al, 2018). Extending these data, Geskin et al (2015) demonstrated that malignant T cells in the skin and blood of CTCL patients express receptors for IL-13.…”

Section: Cellular Interactions Enhance Malignant Stat Activation Promentioning

confidence: 99%

Cellular Interactions and Inflammation in the Pathogenesis of Cutaneous T-Cell Lymphoma

Stolearenco

Namini

Hasselager

et al. 2020

Front. Cell Dev. Biol.

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Cutaneous T-cell lymphoma (CTCL) comprises a group of lymphoproliferative diseases characterized by the accumulation of malignant T cells in chronically inflamed skin lesions. In early stages, the disease presents as skin patches or plaques covering a limited area of the skin and normally follows an indolent course. However, in a subset of patients the cutaneous lesions develop into tumors and the malignant T cells may spread to the lymphatic system, blood and internal organs with fatal consequences. Despite intensive research, the mechanisms driving disease progression remain incompletely understood. While most studies have focused on cancer cell-intrinsic oncogenesis, such as genetic and epigenetic events driving malignant transformation and disease progression, an increasing body of evidence shows that the interplay between malignant T cells and non-malignant cells plays a crucial role. Here, we outline some of the emerging mechanisms by which tumor, stromal and epidermal interactions may contribute to the progression of CTCL with particular emphasis on the crosstalk between fibroblasts, keratinocytes and malignant T cells.

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Interleukin-25 is involved in cutaneous T-cell lymphoma progression by establishing a T helper 2-dominant microenvironment

Abstract: Th2 cytokines highly expressed in CTCL lesional skin induce IL-25 production by epidermal keratinocytes, which may, in turn, lead to formation of a Th2-dominant microenvironment through the direct induction of IL-13 by tumour cells.

Cited by 20 publications

References 40 publications

Targeted genomic analysis of cutaneous T cell lymphomas identifies a subset with aggressive clinicopathological features

Targeted genomic analysis of cutaneous T cell lymphomas identifies a subset with aggressive clinicopathological features

Pruritus as a Distinctive Feature of Type 2 Inflammation

Cellular Interactions and Inflammation in the Pathogenesis of Cutaneous T-Cell Lymphoma

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