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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>
        <description>RSS Feed for Journal of Cutaneous Immunology and Allergy | New and Recent Articles</description>
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        <pubDate>2026-04-09T00:41:18.479+00:00</pubDate>
        <ttl>60</ttl>
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        <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>
      </item><item>
        <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>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15953</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15953</link>
        <title><![CDATA[Cicatricial alopecia of the scalp as a manifestation of IgG4-related disease mimicking acne keloidalis nuchae]]></title>
        <pubdate>2026-01-07T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Ayame Suwayama</author><author>Tomoko Kaminaga</author><author>Shujiro Hayashi</author><author>Shown Tokoro</author><author>Ken Igawa</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15491</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15491</link>
        <title><![CDATA[Modulation of keratinocyte proliferation, migration, and differentiation by calcium and magnesium]]></title>
        <pubdate>2025-12-09T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kazushi Hirakata</author><author>Miyabi Hiyama</author><author>Hideyuki Itabashi</author><author>Akihiko Uchiyama</author><author>Sei-Ichiro Motegi</author>
        <description><![CDATA[BackgroundCalcium and magnesium are essential ions that regulate multiple functions of keratinocytes. However, their precise effects on keratinocyte behavior remain incompletely understood.ObjectivesTo investigate the effects of varying calcium and magnesium concentrations on cell proliferation, migration, and the expression of genes related to differentiation and skin hydration in keratinocytes.MethodsHaCaT cells were stimulated by culture media with various calcium (0.32–18.0 mM) and magnesium concentrations (0.28–8.11 mM). MTT Assay was performed for proliferation. Cell migration ability was observed for 24 h using culture-Insert 2 well. mRNA levels of differentiation-associated gene expression was examined by qPCR assay.ResultsCompared to standard DMEM, lower calcium concentrations and higher magnesium concentrations promoted keratinocyte proliferation. The combination of low calcium and high magnesium additively enhanced cell migration. However, both conditions tended to suppress the expression of genes related to differentiation and moisture retention.ConclusionKeratinocyte functions related to proliferation, migration, and differentiation are intricately regulated by the concentrations of calcium and magnesium, as well as their interactions. Lower calcium and higher magnesium medium might have potential to enhance proliferation and migration in keratinocytes. However, further investigations under in vivo conditions are required to evaluate their effects and to translate these findings into clinical applications.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15763</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15763</link>
        <title><![CDATA[Case Report: Dermatomyositis with symmetrical axillary and inguinal panniculitis associated with anti-NXP-2]]></title>
        <pubdate>2025-12-01T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Eri Uchiyama</author><author>Mei Tochigi</author><author>Yuko Takamiya</author><author>Akira Shimizu</author><author>Takashi Matsushita</author><author>Kazunori Yamada</author>
        <description><![CDATA[We report a rare case of dermatomyositis in a woman in her 60s, presenting with chronic pruritic erythema and symmetrical subcutaneous indurations in both axillae. Physical examination revealed Gottron’s papules and erythematous plaques on the hands and upper extremities. Laboratory tests showed mildly elevated serum CK, aldolase, and CRP levels. CT revealed increased fat density in both axillae, suggestive of panniculitis. Skin and subcutaneous biopsies confirmed interface dermatitis and panniculitis with membranocystic changes. After that, bilateral inguinal panniculitis developed. Autoantibody screening identified strong positivity for anti-NXP-2 and anti-Ki antibodies. Anti-NXP-2 antibody was further confirmed by immunoprecipitation-Western blotting. The diagnosis of dermatomyositis was made, and oral prednisolone (10 mg, 0.2 mg/kg/day) led to marked improvement. These findings may suggest a potential association between anti-NXP-2 antibodies and panniculitis.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15760</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15760</link>
        <title><![CDATA[Diagnostics of cutaneous adverse drug reactions: evaluation of patch tests, lymphocyte transformation tests, and drug provocation tests]]></title>
        <pubdate>2025-11-27T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Tomomu Ishikawa</author><author>Risa Tamagawa-Mineoka</author><author>Koji Masuda</author><author>Norito Katoh</author><author>Takeshi Fukumoto</author>
        <description><![CDATA[BackgroundPatch tests (PT) and/or lymphocyte transformation tests (LTT) are typically performed, when diagnosed with cutaneous adverse drug reactions (CADR). However, their positivity rates can vary depending on the rash type. Additionally, these tests do not always produce positive results, even when the causative drug is used. Conversely, non-specific reactions can occasionally occur.ObjectivesThis study aimed to evaluate the positive rates of PT and LTT for different rash types and to analyze the false-positive and false-negative results of these tests in relation to drug provocation outcomes.MethodsThis was a retrospective descriptive study. The results of PT, LTT, and drug provocation tests for patients diagnosed with CADR at Department of Dermatology, Kyoto Prefectural University of Medicine, from January 2008 to May 2018, were assessed.ResultsA total of 234 patients were diagnosed with CADR, with 43 showing positive reactions to one or more drugs. The highest positivity rate was found in cases of fixed drug eruption. Among the 138 patients who underwent LTT, 44 tested positive for one or more drugs. Drug provocation tests were performed on 31 patients, with 5 exhibiting positive reactions to five drugs. It was observed that three antibiotics produced false-negative results in both PT and LTT. Additionally, antipyretic analgesics yielded false positive results in LTT for 4 patients.ConclusionIt was suggested that the reactivity of PT and LTT could differ based on the rash type. False negatives and false positives might also happen. These factors should be considered when interpreting the test results.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15510</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15510</link>
        <title><![CDATA[Temporal dynamics of cytokine production balance between innate and adaptive lymphocytes in atopic dermatitis model mice]]></title>
        <pubdate>2025-11-20T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Mai Nishimura</author><author>Yoshiaki Matsushima</author><author>Yasutomo Imai</author><author>Keiichi Yamanaka</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15613</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15613</link>
        <title><![CDATA[Changes in biologic treatment patterns for psoriasis before and after the COVID-19 pandemic in Japan; a single center retrospective study]]></title>
        <pubdate>2025-11-17T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Natsumi Ikumi</author><author>Hideki Fujita</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15280</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15280</link>
        <title><![CDATA[Case Report: Blister formation with transient drug hypersensitivity following CAR-T-cell therapy]]></title>
        <pubdate>2025-10-08T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Natsu Watanabe</author><author>Nobuo Kanazawa</author><author>Satoshi Yoshihara</author>
        <description><![CDATA[We present a rare case of a 70-year-old male who developed multiple tense bullae with minimal inflammation after receiving CD19-directed chimeric antigen receptor (CAR)-T-cell therapy for diffuse large B-cell lymphoma. Although strong drug-induced lymphocyte stimulation test positivity was observed initially for multiple drugs, the reactions faded over time. Histopathology revealed subepidermal blistering with minimal inflammatory infiltration, including a mild perivascular infiltration of T lymphocytes, predominantly CD4+ cells rather than CD8+ cells. All of the previously-reported cases with CAR-T-related cutaneous eruptions involve marked inflammation. In contrast, this case may represent a unique blister formation with T-cell hyperreactivity associated with post-CAR-T immune reconstitution. A comparative analysis of previously published cases is provided.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15151</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15151</link>
        <title><![CDATA[The possible effectiveness of difamilast in improving barrier dysfunction in patients with atopic dermatitis and in mouse model]]></title>
        <pubdate>2025-09-22T00:00:00Z</pubdate>
        <category>Original Research</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><![CDATA[Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by pruritus and impaired skin barrier function. Although difamilast, a topical phosphodiesterase-4 (PDE4) inhibitor, has demonstrated clinical efficacy in AD, its role in restoring barrier function remains incompletely understood. This study aimed to investigate the barrier-improving effects of topical difamilast in patients with AD and in an MC903-induced mouse model of AD-like dermatitis. We conducted a retrospective study involving seven Japanese adult patients with mild-to-moderate AD who received 1% difamilast ointment twice daily for 1 week. Transepidermal water loss (TEWL) was measured before and after treatment. Animal experiment was performed using MC903-induced AD-like dermatitis model, followed by treatment with difamilast or vehicle. Dermatitis scores, TEWL, histological changes, immunofluorescence for filaggrin and CD4, and mRNA expression of filaggrin, IL-4, IL-13 and TSLP were evaluated. Topical difamilast reduced TEWL in six out of seven AD patients. In the mouse model, difamilast markedly attenuated dermatitis severity and reduced TEWL. Histological analysis revealed suppression of epidermal thickening and inflammatory cell infiltration. Difamilast restored filaggrin expression and decreased mast cell and CD4+ T-cell infiltration in lesional skin. Quantitative PCR demonstrated that difamilast normalized the MC903-induced decrease in filaggrin and increase in IL-4 mRNA expression. Our findings suggest that difamilast improves skin barrier dysfunction in both human AD and an experimental AD-like mouse model. However, large-scale controlled studies are required to validate its barrier-improving efficacy in real-world clinical settings.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15322</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15322</link>
        <title><![CDATA[Case Report: First reports of Schnitzler syndrome in Iran: clinical presentation and therapeutic challenges]]></title>
        <pubdate>2025-09-11T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Mohammad Aminianfar</author><author>Saeed Soleiman-Meigooni</author><author>Shadi Mohammadi</author><author>Mahdieh Aminianfar</author>
        <description><![CDATA[Schnitzler syndrome (SchS) is a rare, chronic autoinflammatory disorder characterized by a persistent urticarial rash, intermittent fever, arthralgia, bone pain, and elevated systemic inflammatory biomarkers. Due to its diverse manifestations and overlap with other conditions such as hematologic malignancies, connective tissue diseases, and infections, SchS is often underdiagnosed or misdiagnosed, resulting in delayed appropriate treatment. This report delineates the first two documented cases of SchS in Iran. Both patients exhibited pruritic hives, fever, bone pain, and arthralgia. They were initially diagnosed with chronic idiopathic urticaria (CIU). The diagnosis of SchS was confirmed according to the Strasburg criteria, which included a chronic urticarial rash, monoclonal gammopathy, mild interstitial edema, and an interstitial neutrophilic infiltrate without vasculitis, as observed in the histopathological examination of the dermal lesions. Both patients received subcutaneous omalizumab, a disease-modifying antirheumatic drug (DMARD) such as methotrexate, antihistamines, and corticosteroid drugs. We describe their clinical presentations, diagnostic challenges, and therapeutic strategies, emphasizing the limitations encountered in resource-constrained settings, including restricted access to targeted biologic therapies such as interleukin-1 inhibitors. Our findings underscore the importance of heightened clinical vigilance and comprehensive evaluation of atypical urticarial syndromes to facilitate timely diagnosis and improve patient outcomes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15043</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15043</link>
        <title><![CDATA[Two cases of severe childhood-onset psoriasis successfully treated with risankizumab in patients with Down syndrome and morbid obesity]]></title>
        <pubdate>2025-08-14T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Yoshiaki Hara</author><author>Tomomitsu Miyagaki</author><author>Tatsuro Okano</author><author>Takafumi Kadono</author><author>Hidenori Watabe</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15227</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15227</link>
        <title><![CDATA[Association between the neutrophil percentage-to-albumin ratio and generalized pustular psoriasis]]></title>
        <pubdate>2025-08-11T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Arisa Yoshimura</author><author>Shinichi Sato</author><author>Sayaka Shibata</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.14936</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.14936</link>
        <title><![CDATA[Severe lichenified skin rash associated with apalutamide administration]]></title>
        <pubdate>2025-07-22T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Chisato Watanabe</author><author>Shujiro Hayashi</author><author>Shown Tokoro</author><author>Ken Igawa</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15049</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.15049</link>
        <title><![CDATA[Successful conservative management of massive oxaliplatin extravasation from a central venous port with early systemic corticosteroid therapy]]></title>
        <pubdate>2025-07-14T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Shunsuke Takahagi</author><author>Mayu Kanamoto</author><author>Hikari Sakamoto</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.14843</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/jcia.2025.14843</link>
        <title><![CDATA[Two cases of Stevens-Johnson syndrome presenting severe ocular complications associated with immune checkpoint inhibitor]]></title>
        <pubdate>2025-07-10T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Yukiko Nakahara-Omori</author><author>Yukari Kobayashi</author><author>Sumiko Ishizaki</author><author>Kyoko Chujo</author><author>Chikako Suto</author><author>Masaru Tanaka</author><author>Noriko Umegaki-Arao</author>
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