IL-10 promotes Th17 cell differentiation by enhancing STAT1-dependent IL-6 production via IgE-stimulated mast cells.

Mast cells (MCs) are tissue-resident cells of hematopoietic origin that play an important role in host's defense mechanism against nematodes. However, excessive activation of these cells contributes to the development of certain allergic diseases. Immunoglobin E (IgE) is one of the well-known molecules that activate MCs.

[MACULOPAPULAR CUTANEOUS MASTOCYTOSIS HARBORING A KIT MUTATION (ASP419DEL): A CASE REPORT].

A 2-year-old, male patient presented with an 18-month history of scattered, brown macules and nodules up to 2 cm in size on his trunk and extremities. These macules were accompanied by pruritus and were positive for Darier's sign. A skin biopsy of a brown macule on the left thigh revealed a dense accumulation of CD117-positive, round or oval cells with amphophilic cytoplasm within the upper to middle dermis.

[ANALYSIS OF 201 PATIENTS WITH ATOPIC DERMATITIS RECEIVING DUPILUMAB AT TOKYO MEDICAL UNIVERSITY HOSPITAL].

Objective: The present study aimed to assess the course of patients with atopic dermatitis (AD) receiving dupilumab treatment.

Methods: The present, retrospective survey enrolled 201 patients with AD between May 2018 and May 2022 to examine their previous treatment, skin score, percentage of self-injections, EASI improvement rate, treatment continuation rate, number of treatment interruptions, and reasons for the interruptions.

Results: The average EASI severity score was 39.

Topical application of imatinib mesylate suppresses vitamin D3 analog-induced dermatitis in Balb/c mice.

Atopic dermatitis (AD) is an allergic disease mediated by Th2 cells. In AD, externally stimulated keratinocytes release inflammatory cytokines, such as IL-33 and TSLP. Inflammatory cells infiltrate skin tissue and increase vascular permeability.

IL-25 contributes to development of chronic contact dermatitis in C57BL/6 mice, but not BALB/c mice.

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by type 2 immune responses. Interleukin-25 (IL-25) is produced predominantly by epithelial cells. It can activate Th2 cells to produce type 2 cytokines such as IL-4, IL-5 and IL-13, contributing to host defense against nematodes.

Roles of Mast Cells in Cutaneous Diseases.

Mast cells are present in all vascularized tissues of the body. They are especially abundant in tissues that are in frequent contact with the surrounding environment and act as potential sources of inflammatory and/or regulatory mediators during development of various infections and diseases. Mature mast cells' cytoplasm contains numerous granules that store a variety of chemical mediators, cytokines, proteoglycans, and proteases.

[A CHILD CASE OF DIFFUSE CUTANEOUS MASTOCYTOSIS].

Cutaneous mastocytosis (CM) usually appears in childhood and improves substantially before adolescence. The c-KIT mutation of D816V is present in 36% and 20% of patients with childhood-onset CM and diffuse cutaneous mastocytosis (DCM), respectively. In some cases of childhood-onset DCM, the disease can progress to systemic mastocytosis; in others, it resolves spontaneously.

IL-25 exacerbates autoimmune aortitis in IL-1 receptor antagonist-deficient mice.

IL-25, a member of the IL-17 family of cytokines, is known to enhance type 2 immune responses, but suppress type 3 (IL-17A)-mediated immune responses. Mice deficient in IL-1 receptor antagonist (Il1rn mice) have excessive IL-1 signaling, resulting in spontaneous development of IL-1-, TNF- and IL-17A-dependent aortitis. We found that expression of II25 mRNA was increased in the aortae of Il1rn mice, suggesting that IL-25 may suppress development of IL-1-, TNF- and IL-17A-dependent aortitis in Il1rn mice by inhibiting type 3-mediated immune responses.

Recent trends of ocular complications in patients with atopic dermatitis.

Purpose: To elucidate the recent trends in prevalence and characteristics of ocular complications of atopic dermatitis (AD).

Study Design: Cross-sectional observational study.

Methods: Among AD patients who visited our department between 2012 and 2015, 70 patients (140 eyes; recent AD group) who gave informed consent to participate in the study were analyzed.

The roles of IL-17C in T cell-dependent and -independent inflammatory diseases.

IL-17C, which is a member of the IL-17 family of cytokines, is preferentially produced by epithelial cells in the lung, skin and colon, suggesting that IL-17C may be involved in not only host defense but also inflammatory diseases in those tissues. In support of that, IL-17C was demonstrated to contribute to development of T cell-dependent imiquimod-induced psoriatic dermatitis and T cell-independent dextran sodium sulfate-induced acute colitis using mice deficient in IL-17C and/or IL-17RE, which is a component of the receptor for IL-17C. However, the roles of IL-17C in other inflammatory diseases remain poorly understood.

IL-36α is involved in hapten-specific T-cell induction, but not local inflammation, during contact hypersensitivity.

Levels of IL36α are known to be increased in specimens from patients with atopic dermatitis and psoriasis. In addition, it has been reported that IL-36α is crucial for development of imiquimod-induced psoriatic dermatitis in mice. On the other hand, the role of IL-36α in induction of allergic contact dermatitis/contact hypersensitivity (ACD/CHS) is poorly understood.

IL-31 is crucial for induction of pruritus, but not inflammation, in contact hypersensitivity.

IL-31, which is a member of the IL-6 family of cytokines, is produced mainly by activated CD4 T cells, in particular activated Th2 cells, suggesting a contribution to development of type-2 immune responses. IL-31 was reported to be increased in specimens from patients with atopic dermatitis, and IL-31-transgenic mice develop atopic dermatitis-like skin inflammation, which is involved in the pathogenesis of atopic dermatitis. However, the role of IL-31 in development of contact dermatitis/contact hypersensitivity (CHS), which is mediated by hapten-specific T cells, including Th2 cells, is not fully understood.

IL-25 enhances T17 cell-mediated contact dermatitis by promoting IL-1β production by dermal dendritic cells.

Background: In addition to thymic stromal lymphopoietin and IL-33, IL-25 is known to induce T2 cytokine production by various cell types, including T2 cells, T9 cells, invariant natural killer T cells, and group 2 innate lymphoid cells, involved in T2-type immune responses. Because both T2-type and T17-type cells/cytokines are crucial for contact hypersensitivity (CHS), IL-25 can contribute to this by enhancing T2-type immune responses. However, the precise role of IL-25 in the pathogenesis of fluorescein isothiocyanate-induced CHS is poorly understood.

A pulmonary metastatic model of murine melanoma assessed by magnetic resonance imaging.

Immune checkpoint inhibitors and kinase inhibitors have improved prognosis of malignant melanoma (MM) patients. However, these therapies cannot completely overcome the metastasis of MM. Thus, development of new therapy against metastasis should be required.