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        <title>Journal of Cutaneous Immunology and Allergy | New and Recent Articles</title>
        <link>https://www.frontierspartnerships.org/journals/journal-of-cutaneous-immunology-and-allergy</link>
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        <pubDate>2026-09-02T11:46:10.948+00:00</pubDate>
        <ttl>60</ttl>
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        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.17320</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.17320</link>
        <title><![CDATA[Resolution of direct antiglobulin test-negative autoimmune hemolytic anemia without corticosteroid therapy after discontinuation of nivolumab plus ipilimumab therapy for subungual melanoma]]></title>
        <pubdate>2026-09-01T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Michiko Nakajima</author><author>Shintaro Saito</author><author>Mizuki Sato</author><author>Mizuho Nakajima</author><author>Sahori Yamazaki</author><author>Masahito Yasuda</author><author>Sei-ichiro Motegi</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.17346</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.17346</link>
        <title><![CDATA[Case Report: Successful dupilumab treatment for refractory atopic dermatitis-like eczema in a patient with Costello syndrome]]></title>
        <pubdate>2026-08-31T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Toshihiko Nonaka</author><author>Jun Kido</author><author>Mika Ogata</author><author>Taiga Miyake</author><author>Takanobu Yoshida</author><author>Satoshi Fukushima</author><author>Rie Seyama</author><author>Yuri Uchiyama</author><author>Naomichi Matsumoto</author><author>Kimitoshi Nakamura</author>
        <description><![CDATA[Costello syndrome is a rare RASopathy caused by pathogenic variants in HRAS and is characterized by distinctive craniofacial features, growth failure, cardiac abnormalities, tumor predisposition, and various cutaneous manifestations. Although eczema has been reported in patients with Costello syndrome, reports of severe AD-like eczema accompanied by clinically significant allergic manifestations, including food allergy, remain limited. We report a female patient with Costello syndrome caused by a heterozygous HRAS variant, NM_005343.4:c.37G>T, p.(Gly13Cys), who developed severe atopic dermatitis-like eczema and hen’s egg and cow’s milk allergies from infancy. Despite treatment with topical anti-inflammatory agents and emollients, her AD-like eczema remained refractory. Add-on dupilumab therapy was initiated in adolescence, resulting in marked improvement in her skin manifestations within 1 month, and clinical improvement was maintained during subsequent follow-up. This case suggests that dupilumab may be an effective therapeutic option for refractory atopic dermatitis-like eczema associated with Costello syndrome. The clinical course also supports the possible contribution of epithelial-driven type 2 inflammation to severe allergic manifestations in Costello syndrome, although direct mechanistic evidence was not obtained.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.17110</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.17110</link>
        <title><![CDATA[Asymmetrical anhidrosis with hyperpigmentation in a patient with type 1 diabetes]]></title>
        <pubdate>2026-08-28T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Mika Fujiwara</author><author>Tadatsune Iida</author><author>Atsushi Oda</author><author>Hana Takeshita</author><author>Takeshi Namiki</author><author>Naoko Okiyama</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16659</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16659</link>
        <title><![CDATA[Cabozantinib-associated microthrombi causing necrotizing fasciitis-like findings]]></title>
        <pubdate>2026-08-27T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Ichiyo Kawamoto</author><author>Yoshimi Matsuo</author><author>Takumi Sakamoto</author><author>Michiko Kishi</author><author>Tomofumi Numata</author><author>Takanobu Kan</author><author>Akio Tanaka</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.17229</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.17229</link>
        <title><![CDATA[Antinuclear antibody positivity rate and clinical characteristics in prurigo chronica multiformis: a retrospective study of 26 patients]]></title>
        <pubdate>2026-08-18T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kyoko Muraoka</author><author>Yutaka Inaba</author><author>Koki Kayama</author><author>Masatoshi Jinnin</author>
        <description><![CDATA[BackgroundPrurigo chronica multiformis is a refractory chronic pruritic dermatosis that predominantly affects older adults, but the frequency and significance of antinuclear antibody (ANA) positivity remain unclear.MethodsThis retrospective single-center study included 26 patients with prurigo chronica multiformis treated between March 2016 and April 2025. Patients were divided into two groups according to ANA status, and baseline characteristics, allergic background, laboratory investigations, extent of skin involvement, and responsiveness to topical corticosteroids were compared.ResultsFive of 26 patients (19.2%) were positive for ANA. Among evaluable patients, all patients in the positive group showed sensitization to at least one allergen, which was more frequent than in the negative group (100% vs. 37.5%, p = 0.035). The median peripheral blood eosinophil percentage was significantly lower in the positive group (4.0% vs. 8.0%, p = 0.031). No significant differences were observed in the eosinophil count, total IgE levels, extent of skin involvement, or responsiveness to topical corticosteroids.ConclusionApproximately one-fifth of patients with prurigo chronica multiformis were positive for ANA. ANA-positive patients showed a high rate of allergen sensitization and a lower peripheral blood eosinophil percentage. These findings suggest that prurigo chronica multiformis may include an immunologic subtype in which autoimmunity and allergic inflammation intersect.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.17025</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.17025</link>
        <title><![CDATA[A case of Merkel cell carcinoma mimicking cellulitis during Janus kinase inhibitor therapy]]></title>
        <pubdate>2026-08-13T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Takumi Sakamoto</author><author>Takanobu Kan</author><author>Daiki Matsubara</author><author>Akio Tanaka</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16615</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16615</link>
        <title><![CDATA[A case of anti-laminin 332-type mucous membrane pemphigoid with ocular symptoms successfully treated with mycophenolate mofetil and prednisolone in an elderly man]]></title>
        <pubdate>2026-08-11T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Shoko Fukumitsu</author><author>Takashi Hashimoto</author><author>Yukari Matsumoto</author><author>Takayuki Nagai</author><author>Keisuke Iritani</author><author>Yoshiaki Hirako</author><author>Akiharu Kubo</author><author>Takeshi Fukumoto</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.17140</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.17140</link>
        <title><![CDATA[Dissecting cellulitis of the occipital scalp with hair retention within sinus tracts]]></title>
        <pubdate>2026-07-29T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Yuto Yamamura</author><author>Kazuyasu Fujii</author><author>Kazutoshi Nishimura</author><author>Shunya Usui</author><author>Atsushi Otsuka</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16999</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16999</link>
        <title><![CDATA[Low C1q alone should not be taken as diagnostic of acquired angioedema in a kindred with familial type 1 C1-inhibitor deficiency and overlapping systemic lupus erythematosus]]></title>
        <pubdate>2026-07-07T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Amane Takagi</author><author>Saori Takamura</author><author>Tomoo Fukuda</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16781</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16781</link>
        <title><![CDATA[Perioperative anaphylaxis caused by rocuronium bromide: a case series of four patients with skin test confirmation]]></title>
        <pubdate>2026-07-02T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Sayumi Arai</author><author>Nagisa Yoshihara</author><author>Rei Watanabe</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16460</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16460</link>
        <title><![CDATA[Pruritogenic mediators in atopic dermatitis: mechanisms of neurogenic crosstalk]]></title>
        <pubdate>2026-06-03T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Lai-San Wong</author><author>Jen-Hau Yang</author><author>Yu-Ta Yen</author><author>Jenq-Lin Yang</author>
        <description><![CDATA[Pruritus is the most burdensome and persistent symptom of atopic dermatitis (AD), often impairing quality of life more profoundly than visible skin inflammation. Emerging evidence indicates that itch in AD is not merely a downstream consequence of inflammation but an active disease driver that reshapes epidermal barrier integrity and neural plasticity. At the center of AD itch lies a dynamic, bidirectional network linking keratinocytes and sensory neurons. Barrier disruption triggers the release of keratinocyte-derived pruritogens and stress signals that directly activate or sensitize cutaneous nerve fibers, amplifying itch transmission. These epithelial–neuronal interactions are further integrated by intracellular signaling pathways that coordinate environmental and neural inputs. This review synthesizes current mechanistic insights across epidermal and neural compartments and proposes a conceptual framework in which AD itch progresses from peripherally driven signaling to centrally amplified and neurally entrenched states.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16775</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16775</link>
        <title><![CDATA[Remarkable effect of nivolumab on late liver metastasis recurrence in advanced malignant melanoma]]></title>
        <pubdate>2026-05-29T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Shoka Fukuizumi</author><author>Soichiro Kado</author><author>Takayo Ando</author><author>Atsuko Sato</author><author>Koji Kamiya</author><author>Takeo Maekawa</author><author>Mamitaro Ohtsuki</author><author>Mayumi Komine</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16442</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16442</link>
        <title><![CDATA[Real-world effectiveness and safety of tildrakizumab in Japanese patients with psoriasis: a single-center 52-week observational study]]></title>
        <pubdate>2026-05-06T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Daisuke Watabe</author><author>Kanako Tsunoda</author><author>Akemi Hamabata</author><author>Maki Goto</author><author>Wakako Yoshioka</author><author>Hiroo Amano</author>
        <description><![CDATA[BackgroundReal-world data on the long-term effectiveness of tildrakizumab in Japanese patients with psoriasis remain limited, particularly in cohorts with relatively low baseline disease severity.ObjectivesTo evaluate the 52-week effectiveness and safety of tildrakizumab in a real-world Japanese clinical setting, including exploratory subgroup analyses.MethodsThis retrospective, single-center observational study included 30 consecutive patients with psoriasis treated with tildrakizumab 100 mg in accordance with the approved Japanese dosing regimen. Disease severity was assessed using the Psoriasis Area and Severity Index (PASI) at weeks 0, 4, 16, 28, 40, and 52 (visit window ±1 week). Mean PASI scores were analyzed using observed values. For responder analyses, non-responder imputation (NRI) was applied; patients who discontinued treatment or had missing PASI data were classified as non-responders. Responder endpoints included PASI75 and absolute PASI ≤3. Exploratory subgroup analyses were conducted according to baseline characteristics. Statistical analyses were performed using GraphPad Prism.ResultsThe mean PASI score improved from 11.45 at baseline (median 9.2) to 2.90 at week 52. Using NRI, PASI75 and PASI ≤3 achievement rates reached 56.7% and 60.0% at week 52, respectively. Four patients discontinued treatment because of insufficient efficacy, with final PASI scores of 7.5 (week 4), 1.6 (week 16), 3.7 (week 28), and 3.2 (week 40). Twenty-six patients (86.7%) continued treatment through week 52. Seven adverse events were documented during the study period, and no treatment discontinuations related to adverse events occurred.ConclusionTildrakizumab demonstrated sustained real-world effectiveness in Japanese patients with psoriasis, with no treatment discontinuations related to adverse events. Interpretation of the safety and subgroup findings should take into account the retrospective single-center design and exploratory nature of the analyses.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16358</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16358</link>
        <title><![CDATA[Deficiency of inflammatory caspases attenuates IL-33–mediated dermatitis]]></title>
        <pubdate>2026-04-28T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Mami Amaki</author><author>Teruasa Murata</author><author>Nobuo Kanazawa</author><author>Yasutomo Imai</author>
        <description><![CDATA[Interleukin-33 (IL-33) is a nuclear alarmin expressed in epidermal keratinocytes and plays an important role in atopic dermatitis. Environmental stimulation induces extracellular release of IL-33 from the skin. The molecular mechanisms regulating IL-33 release in vivo are not well understood. Previous studies using non-cutaneous tissues or in vitro systems have suggested that IL-33 release is independent of caspase-1. In this study, we examined the role of caspase-1 in IL-33 release from keratinocytes in vivo. Caspase-1 was detected in the nuclei of murine epidermal keratinocytes. After topical stimulation with the hapten 2,4-dinitrofluorobenzene (DNFB), nuclear IL-33 staining in keratinocytes was rapidly lost in wild-type mice. This change was markedly reduced in caspase-1/11–deficient mice. Genetic deletion of caspase-1/11 reduced IL-33–mediated skin inflammation in mice overexpressing IL-33 in keratinocytes, and reduced expression of type 2 cytokines was also observed in the skin. These findings suggest that caspase-1 may play a role in pathogenic IL-33 release in the skin and may control alarmin activity differently across tissues.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16386</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16386</link>
        <title><![CDATA[Immune perturbation in arsenic-induced adverse health effects and cancers]]></title>
        <pubdate>2026-03-30T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Chien-Hui Hong</author><author>Sebastian Yu</author><author>Shu-Li Wang</author><author>Hsin-Su Yu</author><author>Chih-Hung Lee</author>
        <description><![CDATA[Chronic exposure to inorganic arsenic remains a global health concern and is strongly associated with cutaneous malignancies, pigmentation abnormalities, internal cancers, and a range of non-malignant outcomes. In addition to direct genotoxic stress and epigenetic remodeling, arsenic exerts broad immunomodulatory effects that shape disease initiation, persistence, and progression. In the skin, arsenic perturbs barrier integrity, antigen presentation, cytokine networks, and immune surveillance—features that may contribute to the multiplicity and recurrence that characterize arsenic-associated skin cancers. Emerging evidence also highlights the importance of exposure timing (particularly perinatal windows), co-exposures, and host susceptibility factors. This review synthesizes recent advances in: (i) exposure assessment (including noninvasive image-based estimation and biomarker interpretation in the context of diet), (ii) long-latency cancer risk and the population impact of water mitigation, (iii) keratinocyte stress and inflammatory signaling pathways that intersect with cutaneous immune dysregulation, (iv) perinatal metal exposure and allergic disease trajectories with immune profiling, and (v) genetic and epigenetic determinants of susceptibility (including polymorphisms influencing tissue remodeling and arsenic metabolism). We propose an updated framework in which arsenic-driven immune perturbation acts as a unifying axis linking exposure to cutaneous carcinogenesis, internal cancers, and allergic phenotypes, and we outline research gaps and translational opportunities for precision prevention.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16180</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16180</link>
        <title><![CDATA[Case Report: A case with Xeroderma pigmentosum type F manifested a mild phenotype due to a deep intronic variant of the ERCC4 gene]]></title>
        <pubdate>2026-03-20T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Mei Tochigi</author><author>Yuko Takamiya</author><author>Megumi Morita</author><author>Kazushi Anzawa</author><author>Akira Shimizu</author><author>Sumihito Togi</author><author>Hiroki Ura</author><author>Yo Niida</author>
        <description><![CDATA[Xeroderma pigmentosum (XP) is a disorder that causes sun sensitivity, pigmented spots in sun-exposed areas, and neurological symptoms due to an inborn error in the DNA repair process for damage caused by sun exposure. We report a case with XP type F (XPF) diagnosed in a patient in her 70s. We identified that she was homozygous for a deep intronic variant of ERCC4, NC_000016.10(NM_005236.3): c.207+196T>A. This variant causes aberrant mRNA splicing, which confirmed the diagnosis of XP. Seven cases with the same intronic variant have been reported in Japan. In our case, we independently analyzed the qualitative and quantitative aspects of abnormal mRNA splicing, which had not been reported previously, and found approximately 7.7% of the mRNA retained normal splicing. Furthermore, immunostaining of patient’s skin with anti-ERCC4/XP antibody confirmed that the ERCC4 protein was partially expressed rather than being completely absent. This partial expression was predicted to be associated with the relatively mild phenotype observed in our patient.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.15800</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.15800</link>
        <title><![CDATA[The epidemiological and clinical association between primary focal hyperhidrosis and various skin disease in Japanese patients: outpatient questionnaire analysis]]></title>
        <pubdate>2026-02-23T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Keiji Kosaka</author><author>Akihiko Uchiyama</author><author>Mai Ishikawa</author><author>Sei-Ichiro Motegi</author>
        <description><![CDATA[Hyperhidrosis, defined as excessive sweating beyond physiological needs. It impairs the quality of life (QOL) of patients. While there are many studies on the relationship between sweating and skin diseases, however few studies have been conducted from epidemiological perspective of hyperhidrosis on coexisting skin diseases. This study aimed to investigate the prevalence, severity, affected areas, and treatment history of hyperhidrosis among patients with skin diseases. An anonymous, self-report questionnaire was administered to 1,000 patients at the department of dermatology, Gunma University Hospital between June and August 2022, yielding 885 responses (88.5%). Hyperhidrosis was defined using the Hornberger’s diagnostic criteria, and severity was assessed by the Hyperhidrosis Disease Severity Scale (HDSS). The overall prevalence of hyperhidrosis among this skin disease patient cohort was 22.4% (n = 198), which was higher than the rate previously reported in Japan (10%–12.8%). Patients with hyperhidrosis were significantly younger (mean age 51.3 years) than those without (mean age 57.2 years; p < 0.01). Over half (54.3%) of affected patients reported severe or very severe symptoms (HDSS 3 or 4). The most common affected sites were the head/face (15.1%), followed by the axillary (8.7%). The prevalence was high in inflammatory skin diseases, with 29.2% of Atopic Dermatitis (AD) patients, 17.7% of psoriasis patients, and 7.1% of Alopecia Areata (AA) patients also having hyperhidrosis. Despite the high prevalence and severity, only a small fraction of hyperhidrosis patients (7.9%) reported a history of treatment. These findings suggest that hyperhidrosis is a common complication in skin disease. This high prevalence may be attributable to compensatory sweating caused by primary skin diseases. To improve patient’s QOL, dermatologists should actively screen for hyperhidrosis and combine sweat management with skin disease treatment.]]></description>
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        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16328</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16328</link>
        <title><![CDATA[Corrigendum: The possible effectiveness of difamilast in improving barrier dysfunction in patients with atopic dermatitis and in mouse model]]></title>
        <pubdate>2026-02-20T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Akihiko Uchiyama</author><author>Bayarmaa Taivanbat</author><author>Keiji Kosaka</author><author>Mai Ishikawa</author><author>Akihito Uehara</author><author>Masatoshi Shimaoka</author><author>Keiichiro Ryuzaki</author><author>Sei-Ichiro Motegi</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16078</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.16078</link>
        <title><![CDATA[Exacerbation of hand rash after dupilumab initiation in a child with atopic dermatitis who was able to continue treatment]]></title>
        <pubdate>2026-02-05T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Kanoko Kono</author><author>Takashi Sakai</author><author>Yutaka Hatano</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.15453</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2026.15453</link>
        <title><![CDATA[Coexistence of lichenoid and psoriasiform eruptions following PD-1 blockade immunotherapy]]></title>
        <pubdate>2026-01-22T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Tatsuya Ogawa</author><author>Shin Matsumoto</author><author>Keiji Tabuchi</author><author>Toshifumi Nomura</author>
        <description></description>
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