Stratum corneum interleukin-33 expressions correlate with the degree of lichenification and pruritus in atopic dermatitis lesions

Nakamura, Nobutaka; Tamagawa‐Mineoka, Risa; Yasuike, Risa; Masuda, Koji; Matsunaka, Hiroshi; Murakami, Yumi; Yokosawa, Emiko; Katoh, Norito

doi:10.1016/j.clim.2019.02.006

Cited by 29 publications

(27 citation statements)

References 11 publications

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“…Consequently, eosinophils and mast cell infiltration and serum IgE levels were also significantly reduced by alphaIL-33Ab, thus suggesting that blockade of IL-33 negatively influences AD expression. Results obtained from animal models were all confirmed in human cell line studies [57,58,59]. To sum up, it seems that a dysregulation of innate and adaptive immune response could lead to skin damage, which could induce an increased Th2 response (with an upregulated IL-31 and IL-33 production), thus leading to the AD worsening (i.e., scratching, wounding, infections) and progression.…”

Section: Allergic Disordersmentioning

confidence: 67%

IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases

Murdaca

Greco

Tonacci

et al. 2019

IJMS

120

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Several allergic and immunologic diseases including asthma, food allergy (FA), chronic spontaneous urticaria (CSU), atopic dermatitis (AD), systemic lupus erythematosus (SLE), systemic sclerosis (SSc), rheumatoid arthritis (RA), and Behçet’s disease (BD) are characterized by the involvement of Th2 immunity. Several mediators lead to immunoglobulin (Ig)E production, thus including key cytokines such as interleukin (IL)-4, IL-5, and IL-13. Among them, IL-31 and IL-33 have been recently studied as novel biomarkers and future therapeutic targets for allergic and immunological disorders. IL-31 is a proinflammatory cytokine—it regulates cell proliferation and is involved in tissue remodeling. IL-33, acting through its receptor suppression of tumorigenity (ST2L), is an alarmin cytokine from the IL-1 family, whose expression is mediated by tissue damage. The latter has a pleiotropic effect, as it may modulate specific and innate immune cells functions. To date, several researchers have investigated the involvement of IL-31 and IL-33 in several allergic and immune-mediated diseases. Further studies are needed to understand the future applications of these molecules as novel therapeutic agents. This paper aims to give the readers a complete and updated review of IL-31 and IL-33 involvement among the most common autoimmune and allergic disorders.

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Section: Allergic Disordersmentioning

confidence: 67%

IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases

Murdaca

Greco

Tonacci

et al. 2019

IJMS

120

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“…Upon cellular damage or stress, IL-33 is released rapidly as an alarmin to activate the innate immune system [10]. In human AD, IL-33 is abundant in the lesions of epidermal keratinocytes [19][20][21]. However, it is unclear whether IL-33 is the cause or the result of AD.…”

Section: Il-33 In Ad and Other Allergic Disordersmentioning

confidence: 99%

Interleukin-33 in atopic dermatitis

Imai

2019

Journal of Dermatological Science

151

110

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Atopic dermatitis (AD) is characterized by pruritus, barrier disruption, and inflammationincluding type 2 cytokine production. Interleukin-33 (IL-33) is an inflammatory cytokine that is over-expressed in the keratinocytes of patients with AD. IL-33 transgenic mice, which express IL-33 specifically in keratinocytes, spontaneously develop AD-like eczema, suggesting that IL-33 is sufficient for the development of AD. IL-33 stimulates various cells, including group 2 innate lymphoid cells (ILC2s), to produce type 2 cytokines, such as IL-5 and IL-13, and IL-33-stimulated basophils activate ILC2s via IL-4. ILC2s are enriched in human AD skin lesions, and ILC2 isolated from AD lesions, are activated by IL-33, not by thymic stromal lymphopoietin (TSLP). IL-33 induces IL-31, thereby promoting pruritus and scratching behavior. Conversely, scratching the skin promotes IL-33 release from keratinocytes. IL-33 reduces the expression of filaggrin and claudin-1; it also reduces the skin barrier function. However, barrier destruction causes percutaneous exposure to allergens or IL-33 release. Thus, IL-33 is a common point of entry into the itch-scratch cycle of AD. These new findings can facilitate the development of novel therapeutic drugs targeting IL-33.

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“…The effect of substance P to release proinflammatory cytokines from mast cells points to a mechanism how mast cells participate in the neurogenic inflammation in psoriasis and atopic dermatitis as discussed below in more detail. Recently, Nakamura et al (2019) reported increased levels of IL-33 in the stratum corneum of patients with atopic dermatitis. All these data emphasize the role of these cytokines in the context of neuroinflammation and itch, in which mast cells obviously participate.…”

Section: Itch-related Factors Released By Mast Cellsmentioning

confidence: 99%

Mast Cells and Sensory Nerves Contribute to Neurogenic Inflammation and Pruritus in Chronic Skin Inflammation

Siiskonen

Harvima

2019

Front. Cell. Neurosci.

127

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The intimate interaction between mast cells and sensory nerves can be illustrated by the wheal and surrounding flare in an urticarial reaction in human skin. This reaction is typically associated with an intense itch at the reaction site. Upon activation, cutaneous mast cells release powerful mediators, such as histamine, tryptase, cytokines, and growth factors that can directly stimulate corresponding receptors on itch-mediating sensory nerves. These include, e.g., H1-and H4-receptors, proteaseactivated receptor-2, IL-31 receptor, and the high-affinity receptor of nerve growth factor (TrkA). On the other hand, sensory nerves can release neuropeptides, including substance P and vasoactive intestinal peptide, that are able to stimulate mast cells to release mediators leading to potentiation of the reciprocal interaction, inflammation, and itch. Even though mast cells are well recognized for their role in allergic skin whealing and urticaria, increasing evidence supports the reciprocal function between mast cells and sensory nerves in neurogenic inflammation in chronic skin diseases, such as psoriasis and atopic dermatitis, which are often characterized by distressing itch, and exacerbated by psychological stress. Increased morphological contacts between mast cells and sensory nerves in the lesional skin in psoriasis and atopic dermatitis as well as experimental models in mice and rats support the essential role for mast cellsensory nerve communication in consequent pruritus. Therefore, we summarize here the present literature pointing to a close association between mast cells and sensory nerves in pruritic skin diseases as well as review the essential supporting findings on pruritic models in mice and rats.

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Stratum corneum interleukin-33 expressions correlate with the degree of lichenification and pruritus in atopic dermatitis lesions

Cited by 29 publications

References 11 publications

IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases

IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases

Interleukin-33 in atopic dermatitis

Mast Cells and Sensory Nerves Contribute to Neurogenic Inflammation and Pruritus in Chronic Skin Inflammation

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