The ambiguous pruritogenic role of interleukin-31 in cutaneous T-cell lymphomas in comparison to atopic dermatitis: a review

Olszewska, Berenika; Sokołowska‐Wojdyło, Małgorzata; Lakomy, Joanna; Nowicki, Roman

doi:10.5114/ada.2020.96260

Cited by 7 publications

(6 citation statements)

References 56 publications

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“…It has been hypothesized that IL-31 may induce epidermal neoplastic T cells and keratinocytes to transmit itch, indirectly affecting sensory nerves (54). Although IL-31 appears to have a role in pruritus in CTCL, there is conflicting evidence as to whether it plays a larger role in the pathogenesis of CTCL itself (56,58,59). However, of note, chronic prurigo has also been reported in cases of Hodgkin lymphoma (HL) (60), and a study in HL patients demonstrated elevated IL-31 in HL cells and in the immune cells infiltrating affected lymph nodes (61).…”

Section: Cutaneous T-cell Lymphoma (Ctcl)mentioning

confidence: 99%

Interleukin-31 as a Clinical Target for Pruritus Treatment

Kabashima

Irié

2021

Front. Med.

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In recent years, the published literature has suggested the key involvement of the cytokine interleukin-31 (IL-31) in the symptomatology of pruritus, and both IL-31 and its receptor have become potential therapeutic targets for a range of pruritic diseases. Elevated levels of IL-31 or its receptor have been reported in the tissue or serum of patients with pruritic skin diseases, such as atopic dermatitis, prurigo nodularis, and psoriasis. Pruritus places a heavy burden on patients, and can have a negative impact on daily life, sleep, and mental health. Since current anti-pruritic treatments are often ineffective, affected patients are in urgent need of new therapies. As a result, drug development targeting the IL-31 pathway is evolving rapidly. To date, only nemolizumab, a humanized monoclonal antibody targeting the IL-31 receptor, has successfully completed late-stage clinical studies. This article will highlight our current clinical understanding of the role of IL-31 in pruritic disease, and explore recent progress in drug development as well as the anticipated future advances in this field.

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Section: Cutaneous T-cell Lymphoma (Ctcl)mentioning

confidence: 99%

Interleukin-31 as a Clinical Target for Pruritus Treatment

Kabashima

Irié

2021

Front. Med.

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“…The most studied model was CTCL, where the pathogenetic mechanism seems to be emblematic. The researches collected together with other reports were not able to clarify if interleukin 31 is connected to the itch, to the cancer or to both [ 42 ]. These data are encouraging in respect to a potential anti-pruritic treatment based on reducing IL-31 or its receptor IL-31RA.…”

Section: Discussionmentioning

confidence: 99%

IL-31, itch and hematological malignancies

et al. 2021

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Pruritus is one of the most common symptoms experienced by neoplastic patients. The pathogenesis of neoplastic itch is complex and multifactorial and could be due to an unbalanced production of humoral mediators by altered immune effector cells. IL-31 is a pro-inflammatory cytokine produced by CD4 + T helper cells. The aim of this review was to evaluate the role of this Th2 cytokine and its receptor IL-31RA, in the onset of neoplastic pruritus. We analysed scientific literature looking for the most relevant original articles linking IL-31to itch in oncologic diseases. Interleukin-31 seems to be a main itch mediator in several hematologic disease such as Cutaneous T cells lymphomas. In these patients IL-31 was positively linked to itch level, and IL-31 matched with disease stage. IL-31 seems to play an important role in the signalling pathway involved in pruritus, but it is also suggested to play a proinflammatory and immunomodulatory role which could play a part in the progression of the neoplastic disease. Further studies will be fundamental in facing pruritus in oncologic patients, since this problem compromise their quality of life worsening an already critic picture.

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“…82,83 As a major product of CD4 + T cells in DOCK8 deficient mice, IL-31 appears to be involved in the DOCK8 mutation-driven hyper IgE syndrome, characterized by a combined immunodeficiency, eczematous skin lesion, and high serum IgE levels. 84 Finally, initial, yet mostly descriptive or non-controlled and small scale human studies/trials suggest an involvement of IL-31 in various cutaneous disorders beyond AD including pemphigus herpetiformis, 85 chronic spontaneous urticaria, 86,87 cutaneous T-cell lymphoma, [88][89][90][91][92] systemic lupus erythematosus, 93,94 bullous pemphigoid, [95][96][97] dermatomyositis, 98 and psoriasis. 70,[99][100][101][102] This needs to be further explored, especially given the potential beneficial effect of new anti-IL-31 strategies in these sometimes hard-to-treat skin diseases.…”

Section: The Il-31 Axis In the Skinmentioning

confidence: 99%

“…Finally, initial, yet mostly descriptive or non‐controlled and small scale human studies/trials suggest an involvement of IL‐31 in various cutaneous disorders beyond AD including pemphigus herpetiformis, 85 chronic spontaneous urticaria, 86,87 cutaneous T‐cell lymphoma, 88–92 systemic lupus erythematosus, 93,94 bullous pemphigoid, 95–97 dermatomyositis, 98 and psoriasis 70,99–102 . This needs to be further explored, especially given the potential beneficial effect of new anti‐IL‐31 strategies in these sometimes hard‐to‐treat skin diseases.…”

Section: Introductionmentioning

confidence: 99%

Interleukin‐31: The “itchy” cytokine in inflammation and therapy

Datsi

Steinhoff

Faried

et al. 2021

Allergy

122

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The cytokine interleukin-31 has been implicated in the pathophysiology of multiple atopic disorders such as atopic dermatitis (AD), allergic rhinitis, and airway hyperreactivity. In AD, IL-31 has been identified as one of the main "drivers" of its cardinal symptom, pruritus. Here, we summarize the mechanisms by which IL-31 modulates inflammatory and allergic diseases. T H 2 cells play a central role in AD and release high levels of T H 2-associated cytokines including IL-31, thereby mediating inflammatory responses, initiating immunoregulatory circuits, stimulating itch, and neuronal outgrowth through activation of the heterodimeric receptor IL-31 receptor A (IL31RA)/ Oncostatin M receptor (OSMRβ). IL31RA expression is found on human and murine dorsal root ganglia neurons, epithelial cells including keratinocytes and various innate immune cells. IL-31 is a critical cytokine involved in neuroimmune communication, which opens new avenues for cytokine modulation in neuroinflammatory diseases including AD/pruritus, as validated by recent clinical trials using an anti-IL-31 antibody. Accordingly, inhibition of IL-31-downstream signaling may be a beneficial approach for | 2983 DATSI eT Al.

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The ambiguous pruritogenic role of interleukin-31 in cutaneous T-cell lymphomas in comparison to atopic dermatitis: a review

Cited by 7 publications

References 56 publications

Interleukin-31 as a Clinical Target for Pruritus Treatment

Interleukin-31 as a Clinical Target for Pruritus Treatment

IL-31, itch and hematological malignancies

Interleukin‐31: The “itchy” cytokine in inflammation and therapy

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