Abstract
Background:
Toripalimab in combination with cisplatin and paclitaxel is indicated as a first-line treatment for metastatic esophageal squamous cell carcinoma (ESCC). Toripalimab, a PD-1 inhibitor, commonly causes immune-related adverse reactions such as immune-related rash, immune-related pneumonitis, and immune-related diarrhea and colitis. This study reports a case of toripalimab-induced exacerbation of psoriasis in an esophageal cancer patient, emphasizing the need for careful monitoring and management in such treatments.
Case presentation:
A 60-year-old male patient with a history of well-controlled psoriasis without medication and no other significant medical conditions was hospitalized due to recurrence and exacerbation of psoriasis following two cycles of Toripalimab combined with cisplatin and nab-paclitaxel therapy after esophageal malignancy surgery. The psoriasis flare-up was considered to be induced by Toripalimab. After admission, the patient was treated with high-dose methylprednisolone. Upon symptom control, the steroid dosage was gradually tapered and completely discontinued over a total course of approximately eight weeks, with no recurrence throughout the tapering and discontinuation period.
Conclusion:
For cancer patients with pre-existing autoimmune diseases, particularly those with psoriasis, comprehensive multidisciplinary evaluation is essential before initiating Toripalimab therapy. During immunotherapy cycles, specialized follow-up by dermatologists and clinical pharmacists is recommended to monitor the status of pre-existing dermatological conditions and potential adverse reactions.
Introduction
Toripalimab, the first domestically developed PD-1 inhibitor in China, has become a crucial therapeutic option for advanced malignancies including melanoma and esophageal squamous cell carcinoma since its approval in China in 2018 (). Toripalimab is a humanized IgG4 monoclonal antibody that specifically binds to the PD-1 receptor on the surface of T cells. By blocking the interaction between PD-1 and its ligands PD-L1/PD-L2 on tumor cells, it alleviates the immunosuppressive effects of the tumor microenvironment, thereby restoring T cells’ ability to recognize and eliminate tumor cells (, ).
Psoriasis is a chronic, immune-mediated inflammatory skin disease (). A systematic, worldwide review found the prevalence of psoriasis ranged from 0.5 to 11.4 percent in adults and 0 to 1.4 percent in children (). The etiology of psoriasis is multifactorial, with medication exposure being a significant external contributing factor (). Currently, case reports have indicated that nivolumab, pembrolizumab, durvalumab, and atezolizumab may induce or exacerbate psoriasis ().While the specific mechanisms underlying ICI-induced psoriasis remain controversial, the overexpression of Th1/Th17-specific cytokines, such as IL-17, following blockade of PD-1 may be involved ().Our case provides the first documented evidence of Toripalimab-induced psoriasis flare in a patient with esophageal cancer. This case underscores the need to screen for psoriasis history before Toripalimab initiation, as pre-existing autoimmune conditions may heighten flare risk. Clinicians should monitor psoriasis patients on toripalimab for paradoxical worsening, even if baseline disease is quiescent.
Case description
We describe a 60-year-old male patient presenting with progressive postprandial dysphagia. Gastroscopic examination confirmed esophageal malignancy, while contrast-enhanced chest CT demonstrated: (1) carcinoma at the lower esophagus with periesophageal and mediastinal lymphadenopathy; (2) multiple subcentimeter lymph nodes in bilateral supraclavicular regions, lesser omental sac, and retroperitoneum, raising suspicion of metastatic dissemination. On October 16, 2024, the patient underwent “radical esophagectomy via a right thoracic approach combined with laparotomy” under general anesthesia. The postoperative pathological findings of the patient indicate: (Esophagus, lower segment) Medullary type squamous cell carcinoma (tumor size: 2.4×2×2 cm) with moderate differentiation. The tumor infiltrates into the superficial muscular layer, with visible vascular tumor emboli and perineural invasion. Lymph node metastasis: 10/24 lymph nodes showed metastatic carcinoma: perigastric: 4/11 nodes, para-azygous: 0/1 node, diaphragmatic crus: 1/4 nodes, inferior pulmonary vein: 1/1 node, subcarinal: 4/7 nodes. Both proximal and distal resection margins are negative. Final pathological staging: pT2N3Mx. The patient had a 40-year history of alcohol consumption and a 5-year smoking history, and had abstained from both smoking and alcohol since undergoing surgery. The patient had a 20-year history of psoriasis, yet no psoriatic plaques were documented during the baseline dermatological assessment prior to ESCC treatment initiation. The patient had no other significant past medical history, with hepatic and renal functions otherwise within normal limits.
Baseline evaluation prior to treatment initiation revealed a body mass index of 20.82 kg/m², Nutritional Risk Screening (NRS) 2002 score of 2 (indicating moderate nutritional risk), and Eastern Cooperative Oncology Group (ECOG) performance status grade 1 (fully ambulatory).The patient initiated combination therapy with Albumin-bound paclitaxel 400mg Day 1 + Toripalimab 240mg Day 1 + Cisplatin 30mg Days 1–3 on November 20, 2024, and December 13, 2024. During chemotherapy, the patient received comprehensive supportive care including omeprazole for stress ulcer prophylaxis, compound glycyrrhizin for hepatoprotection, ondansetron and/or metoclopramide as antiemetic agents, and human granulocyte colony-stimulating factor (G-CSF) for neutropenia prophylaxis. Approximately 10 days after the completion of the second cycle, the patient developed generalized rash with desquamation accompanied by pruritus, but no pain. The dermatologist prescribed Xiaoyin Capsules, Compound Glycyrrhizin, and Halometasone and Triclosan Cream to alleviate symptoms. However, the symptoms showed inadequate improvement, and the patient was subsequently hospitalized for further treatment on January 10, 2025. Figure 1 provides a comprehensive illustration of the patient’s detailed treatment process.
Figure 1
Upon hospital admission, the patient was conscious and alert, with vital signs including temperature and blood pressure within normal ranges. Multiple plaques of varying sizes, well-demarcated, irregularly shaped, and erythematous were observed on the trunk and extremities, covered with thick scales. Some lesions coalesced into patches, with a positive Auspitz sign. The patient reported pruritus but no pain (Figure 2). Based on the clear clinical presentation, the patient was diagnosed with an exacerbation of psoriasis vulgaris. According to the patient’s medication history and the Naranjo Adverse Drug Reaction Probability Scale, it has been concluded that the exacerbation is attributed to toripalimab. The patient was treated with methylprednisolone 40 mg every 12 hours for 4 days, in accordance with the guidelines for immune checkpoint inhibitor-related adverse events (, ). The systemic desquamative rash and pruritus showed improvement compared to previous status. The treatment was then switched to methylprednisolone 40 mg once daily for 3 days, followed by gradual tapering to a maintenance dose of methylprednisolone 20 mg once daily orally.
Figure 2
After exclusion of chemotherapy contraindications, the patient received chemotherapy regimens on January 19, 2025 and February 9, 2025 as follows: Albumin-bound paclitaxel 400mg on Day 1 + Cisplatin 30mg on Days 1-3. The immunotherapy was ceased in view of the psoriatic flare. The patient reported no discomfort during treatment. Upon admission on February 9, the dose of methylprednisolone had been tapered to 12mg once daily. Skin lesions on the trunk and limbs showed significant improvement compared to previous assessments, with only a few residual plaques visible (as shown in Figure 3). The patient successfully discontinued methylprednisolone through a stepwise tapering protocol without psoriasis recurrence during the withdrawal period or subsequent surveillance.
Figure 3
Discussion
Per Naranjo criteria, the likelihood of drug-induced psoriasis exacerbation was graded as probable for toripalimab (score=5) and possible for both albumin-bound paclitaxel and cisplatin (scores=1 each). We hypothesize that toripalimab was the trigger to the psoriasis exacerbation in our patient.
Immune checkpoint inhibitors (ICIs) are a groundbreaking advancement in cancer treatment, offering patients hope through their remarkable effectiveness. However, it is essential to recognize that, alongside these significant benefits, ICIs can lead to a range of immune-related side effects (irAEs). Non-specific maculopapular rash, pruritus, lichenoid reactions, eczema, and vitiligo are the most common dermatologic side effects (). It has been reported that ICI-associated psoriasis or psoriasiform reactions accounted for 3.8% of all cutaneous toxicities in the EudraVigilance drug safety database (). There have been increasing reports of cases where ICIs nivolumab and pembrolizumab triggered or exacerbated psoriasis (–). In the review by Liliana Gabriela Popa, in addition to nivolumab and pembrolizumab, durvalumab and atezolizumab have also been reported to induce or exacerbate psoriasis ().
In a systematic review of 242 cases of ICI-mediated psoriasis (including five cases with the inverse phenotype), the mean numbers of ICI cycles prior to ICI-induced de novo or flare of pre-existing psoriasis were 9.9 cycles and 6.4 cycles, respectively (). However, this case report shows that the patient developed severe psoriasis exacerbation after completing two cycles of toripalimab therapy. We hypothesized a potential correlation between the patient’s chronic alcohol consumption and smoking history. Accumulating clinical evidence has established smoking as a significant independent risk factor for psoriasis recurrence (P<0.05) (). Furthermore, longitudinal cohort studies demonstrated that various smoking phenotypes - particularly smoking initiation age, cigarettes-per-day intensity, and cumulative pack-years-consistently show dose-dependent positive associations with psoriasis risk (OR>1,P<0.05) (). Clinical evidence confirms a dose-dependent positive association between alcohol consumption and psoriasis incidence, with high-dose intake (>45 g/day) significantly elevating disease susceptibility ().Given the patient’s brief abstinence duration (only 1 month smoking/alcohol cessation) prior to toripalimab initiation, it is mechanistically plausible that pre-existing alcohol and tobacco exposure histories may have potentially exacerbated psoriatic progression during anti-PD-1 therapy. Analysis of concomitant medications during the patient’s chemotherapy revealed that G-CSF may contribute to immune evasion by suppressing T-cell function and promoting differentiation of immunosuppressive cells (, ). Given that psoriasis is a Th17-mediated autoimmune disorder, this mechanism theoretically carries the potential to exacerbate psoriatic inflammation. However, there is a lack of direct clinical evidence.
Although a possible rationale for the pathogenesis can be proposed, this remains speculative. Psoriasis is recognized as a T-cell- and dendritic-cell-mediated disease. IL-17 and IL-22 produced by T helper (Th) 1, 17, and 22 cells play a central role in its pathophysiology ().The PD-1 pathway physiologically downregulates Th cell activity. PD-1 inhibitors exert their effects by blocking PD-1/PD-L1 interactions, thereby reversing T cell suppression and resulting in hyperactivation of psoriasis-associated Th1/Th17 subsets accompanied by dysregulated cytokine production ().These activated T cells secrete various cytokines including interferon-γ, IL-1, IL-17, and IL-22 (),which subsequently migrate to cutaneous tissues and activate resident immune cells (keratinocytes, dendritic cells, and neutrophils), ultimately inducing or aggravating psoriatic lesions ().
Upon IL-17 stimulation, keratinocytes exhibit effector functions by autonomously releasing VEGF, S100 proteins, antimicrobial peptides, and chemokines. This cytokine milieu facilitates the recruitment of additional immune cells (e.g., neutrophils) and establishes a self-perpetuating inflammatory cascade that sustains psoriatic plaques (, ). Pharmacological inhibition of the PD-1 pathway specifically enhances Th17 responses (), providing a mechanistic explanation for psoriasis exacerbation observed during toripalimab therapy. Furthermore, PD-1 blockade-induced psoriasiform dermatitis is histologically characterized by prominent epidermal infiltration of CD8+ T cells and overexpression of IL-6, IL-23, and IL-17A cytokines (). Martina Morelli also found that IL-6 and TNF-α are aberrantly expressed in psoriasis reactions induced by anti-PD-1, at levels comparable with chronic psoriasis (). At the molecular level, TRIM14 upregulation promotes TRAF3 degradation via NDP52-mediated autophagy, relieving NF-κB pathway inhibition and exacerbating inflammation ().The recurrence of psoriasis may be closely associated with tissue-resident memory T (Trm) cells persisting within clinically healed lesions. These cells are reactivated following immune checkpoint inhibitor (ICI) administration, secreting pro-inflammatory cytokines such as IL-17A/F, ultimately leading to recurrence in the original lesional areas (, ).Research shows that toripalimab binds to the FG loop of PD-1 with 12-fold higher affinity than pembrolizumab, resulting in enhanced T cell activation (including amplified Th1 and myeloid inflammatory responses) (). This mechanism may potentially influence the intensity of irAEs.
The management of irAEs, as per the European Society for Medical Oncology (ESMO), Chinese Society of Clinical Oncology(CSCO) guidelines, is based on Common Terminology Criteria for Adverse Events (CTCAE) toxicity grading. For grades 3 toxicities, immunotherapy should be withheld until resolution to grade 0–1, with permanent discontinuation considered if no improvement occurs within 12 weeks. High-dose corticosteroids must be initiated promptly, and additional immunosuppressive agents (e.g., infliximab, mycophenolate mofetil, or cyclophosphamide) should be introduced if clinical deterioration persists under steroid therapy (–).
In our case, multiple erythematous plaques with varying sizes, well-demarcated borders, and irregular configurations were observed on the patient’s trunk and extremities, exhibiting thick, adherent scales. The Psoriasis Area and Severity Index(PASI)score was 21.8, with >30% body surface area (BSA) involvement. Grade 3 toxicity was confirmed by multidisciplinary evaluation, leading to toripalimab discontinuation and immediate intravenous methylprednisolone (40 mg every 12 hours). Post-treatment, the PASI score declined to 1.8 with <5% BSA involvement, demonstrating marked improvement.
Notably, the American Academy of Dermatology-National Psoriasis Foundation (AAD-NPF) opposes corticosteroid use for de novo or PD-1 inhibitor-exacerbated psoriasis due to risks of relapse during tapering and limited sustained efficacy ().Kim A. Papp noted that glucocorticoids are commonly used in oncology to control early stages of irAEs, but not typically used by dermatologists to treat psoriasis because of long-term risks and the potential for disease flares upon glucocorticoids cessation ().Given the strong endorsement of glucocorticoids for immune-related cutaneous toxicities by ESMO/CSCO/CCO/SITC guidelines, this intervention was prioritized. The patient achieved sustained remission without psoriasis recurrence after steroid withdrawal, supporting its selective utility in irAE management.
Conclusion
To the best of our knowledge, this is the first evidence of psoriasis exacerbation in ESCC patients receiving toripalimab treatment. We suggest that prior to initiating PD-1/PD-L1, assessment for preexisting autoimmune conditions or family history of autoimmune disorders must be prioritized. Particularly for patients with documented psoriasis history, dermatologists should perform archival skin biopsies, while clinical pharmacists comprehensively evaluate prior immunomodulatory drug usage to verify completion of appropriate washout periods. During treatment, regular multidisciplinary follow-up is recommended to monitor cutaneous and systemic adverse reactions, with adverse event management strictly following CTCAE grading criteria. We will further investigate biomarkers such as IL-17 to determine whether specific laboratory assays can definitively assess the effects of immune checkpoint inhibitors in psoriasis patients with prior history of the disease.
Statements
Data availability statement
The original contributions presented in the study are included in the article/supplementary material. Further inquiries can be directed to the corresponding author.
Ethics statement
Ethical approval for this study was obtained from the local institutional ethics committee. Written informed consent was obtained from the individual for the publication of any potentially identifiable images or dataincluded in this article.
Author contributions
LZ: Writing – original draft, Writing – review & editing. ZC: Writing – review & editing. PL: Writing – review & editing.
Funding
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References
1
National Medical Products Administration. Toripalimab, the first domestic anti-PD-1 monoclonal antibody, was approved into market (2018). Available online at: https://www.nmpa.gov.cn/directory/web/nmpa/zhuanti/ypqxgg/gggzjzh/20181217161101989.html (Accessed November 30, 2021).
2
KeamSJ. Toripalimab: first global approval. DRUGS. (2019) 79:573–8. doi: 10.1007/s40265-019-01076-2
3
ZhangLHaoBGengZGengQ. Toripalimab: the first domestic anti-tumor PD-1 antibody in China. Front Immunol. (2022) 12:730666. doi: 10.3389/fimmu.2021.730666
4
BoehnckeWHSchonMP. Psoriasis. Lancet. (9997) 2015:386. doi: 10.1016/S0140-6736(14)61909-7
5
MichalekIMLoringBJohnSM. A systematic review of worldwide epidemiology of psoriasis. J Eur Acad Dermatol. (2017) 31:205–12. doi: 10.1111/jdv.13854
6
BalakDMHajdarbegovicE. Drug-induced psoriasis: clinical perspectives. Psoriasis (Auckl). (2017) 7:87–94. doi: 10.2147/PTT.S126727
7
PappKAPuigLBeeckerJChandrannVClaveauJCortésJet al. Systemic treatment of immune checkpoint inhibitor-induced psoriasis: Inference-based guidance. J Eur Acad Dermatol Venereol. (2025) 6. doi: 10.1111/jdv.20809
8
DulosJCarvenGJvan BoxtelSJEversSDriessen-EngelsLJAHoboWet al. PD-1 blockade augments Th1 and Th17 and suppresses Th2 responses in peripheral blood from patients with prostate and advanced melanoma cancer. J Immunother. (2012) 35:169–78. doi: 10.1097/CJI.0b013e318247a4e7
9
BrahmerJRAbu-SbeihHAsciertoPABrufskyJCappelliLCCortazarFBet al. Society for Immunotherapy of Cancer (SITC) clinical practice guideline on immune checkpoint inhibitor-related adverse events. J Immunother Cancer. (2021) 9:e002435. doi: 10.1136/jitc-2021-002435
10
Respiratory Physician Branch of Chinese Medical Doctor Association. Multidisciplinary Diagnosis and Treatment Professional Committee of Chinese Medical Doctor Association. Recommendations for prevention and management of immune checkpoint inhibitor-related toxicities. Natl Med J China. (2022) 102:1811–32. doi: 10.3760/cma.j.cn112137-20211221-02842
11
SibaudVMeyerNLamantLVigariosEMazieresJDelordJP. Dermatologic complications of anti-PD1/PD-L1 immune checkpoint antibodies. Curr Opin Oncol. (2016) 28:254–63. doi: 10.1097/CCO.0000000000000290
12
CutroneoPIngrasciottaYIsgròVRulloEVBerrettaMFioricaFet al. Psoriasis and psoriasiform reactions secondary to immune checkpoint inhibitors. Dermatol Ther. (2021) 34:e14830. doi: 10.1111/dth.14830
13
MullangiSPonnamSLekkalaMRKoyaS. A case of de novo psoriasis secondary to nivolumab in a patient with metastatic renal cell carcinoma. Cureus. (2021) 13:e15703. doi: 10.7759/cureus.15703
14
MonsourEPPothenJBalaramanRA. Novel approach to the treatment of pembrolizumab-induced psoriasis exacerbation: A case report. Cureus. (2019) 11:e5824. doi: 10.7759/cureus.5824
15
Mayor IbargurenAEnriqueEADianaPLAnaCPedroHP. Apremilast for immune checkpoint inhibitor-induced psoriasis: A case series. JAAD Case Rep. (2021) 11:84–9. doi: 10.1016/j.jdcr.2021.03.015
16
ZhaoSSunWSunJPengLWangC. Clinical features, treatment, and outcomes of nivolumab induced psoriasis. Invest New Drug. (2023). doi: 10.1007/s10637-024-01494-4
17
ShoukfehRYassineRTurkDMoossaviMNofzingerA. New-onset psoriasis induced by durvalumab. Cureus. (2023) 15:e48453. doi: 10.7759/cureus.48453
18
SicilianoMADastoliSd’ApolitoMStaropoliNTassonePTagliaferriPet al. Pembrolizumab-induced psoriasis in metastatic melanoma: activity and safety of apremilast, a case report. Front Oncol. (2020) 10:579445. doi: 10.3389/fonc.2020.579445
19
PopaLGGiurcaneanuCPortelliMGMihaiMMBeiuCOrzanOAet al. Perspectives on psoriasiform adverse events from immune checkpoint inhibitors: lessons learned from our practice. MEDICINA-LITHUANIA. (2023) 60:1–19. doi: 10.3390/medicina60030373
20
SaidJTElmanSAPerez-ChadaLMMitaCMerolaJFLeBoeufNR. Treatment of immune checkpoint inhibitor-mediated psoriasis: A systematic review. J Am Acad Dermatol. (2022) 87:399–400. doi: 10.1016/j.jaad.2022.02.030
21
ShenFDingYQiangYDuanZXuQGaoXet al. Tobacco Smoking Was Positively Associated with Disease Relapse at week 24 and 48 Among Patients with Psoriasis Vulgaris in Shanghai: A Prospective Study. Psoriasis (Auckl). (2025) 15:261–72. doi: 10.2147/PTT.S534032
22
KimSRChoiYGJoSJ. Effect of smoking cessation on psoriasis vulgaris, palmoplantar pustulosis and generalized pustular psoriasis. Br J Dermatol. (2024) 191:225–32. doi: 10.1093/bjd/ljae130
23
ChoiJHanIMinJYunJKimBSShinKet al. Dose-response analysis between alcohol consumption and psoriasis: A systematic review and meta-analysis. J der Deutschen Dermatologischen Gesellschaft = J German Soc Dermatology: JDDG vol. (2024) 22:5. doi: 10.1111/ddg.15380
24
BleuzéMLavoieJPBédardCGottschalkMSeguraM. Encapsulated Streptococcus suis impairs optimal neutrophil functions which are not rescued by priming with colony-stimulating factors. PloS One. (2024) 19:e0296844. doi: 10.1371/journal.pone.0296844
25
ParkYChungC. Immune evasion of G-CSF and GM-CSF in lung cancer. Tuberculosis Respir Dis. (2024) 87:22–30. doi: 10.4046/trd.2023.0037
26
MahilSKCaponFBarkerJN. Update on psoriasis immunopathogenesis and targeted immunotherapy. Semin Immunopathol. (2016) 38:11–27. doi: 10.1007/s00281-015-0539-8
27
WanZHuangJOuXLouSWanJShenZ. Psoriasis de novo or exacerbation by PD-1 checkpoint inhibitors. Anais brasileiros dermatologia. (2024) 99:425–32. doi: 10.1016/j.abd.2023.09.003
28
EshaqAMFlanaganTWBa AbbadAAMakaremZAABokirMSAlasheqAKet al. Immune checkpoint inhibitor-associated cutaneous adverse events: mechanisms of occurrence. Int J Mol Sci. (2023) 26:1–33. doi: 10.3390/ijms26010088
29
ZengWWangYCaoYXingFYangX. Study of dietary−induced progression of psoriasis−like mice based on gut macrophage polarization. Exp Ther Med. (2023) 25:278. doi: 10.3892/etm.2023.11976
30
KamataMTadaY. Crosstalk: keratinocytes and immune cells in psoriasis. Front Immunol. (2023) 14:1286344. doi: 10.3389/fimmu.2023.1286344
31
YangWHeRQuHLianWXueYWangTet al. FXYD3 enhances IL-17A signaling to promote psoriasis by competitively binding TRAF3 in keratinocytes. Cell Mol Immunol. (2023) 20:292–304. doi: 10.1038/s41423-023-00973-7
32
MatsumuraNOhtsukaMKikuchiNYamamotoT. Exacerbation of psoriasis during nivolumab therapy for metastatic melanoma. Acta Derm Venereol. (2016) 96:259–60. doi: 10.2340/00015555-2212
33
TanakaRIchimuraYKubotaNSaitoANakamuraYIshitsukaYet al. Activation of CD8 T cells accelerates anti-PD-1 antibody-induced psoriasis-like dermatitis through IL-6. Commun Biol. (2020) 3:571–82. doi: 10.1038/s42003-020-01308-2
34
MorelliMCarboneMLScaglioneGLScarponiCDi FrancescoVPallottaSet al. Identification of immunological patterns characterizing immune-related psoriasis reactions in oncological patients in therapy with anti-PD-1 checkpoint inhibitors. Front Immunol. (2023) 15:1346687. doi: 10.3389/fimmu.2024.1346687
35
LiMLiDZhangYWangJWangSZhaoHet al. Cannabidiol-loaded hydrogel microneedle patches inhibit TRIM14/TRAF3/NF-κB axis for the treatment of psoriasis. Int J Biol macromolecules. (2025) 304:140825. doi: 10.1016/j.ijbiomac.2025.140825
36
PengLLiuWChengYChenLShenZ. IL-17A/F double producing T cells, unstable Tregs and quiescent TRMs in clinically healed lesions are potential cellular candidates for recurrence of psoriasis. Clin Immunol (Orlando Fla.). (2024) 266:110328. doi: 10.1016/j.clim.2024.110328
37
Saavedra-AlmarzaJMalgueFGarcía-GómezMGouëtSEdwardsNPalmaVet al. Unveiling the role of resident memory T cells in psoriasis. J leukocyte Biol. (2025) 117:qiae254. doi: 10.1093/jleuko/qiae254
38
RajasekaranNWangXRavindranathanSChinDJTsengSYKlakampSLet al. Toripalimab, a therapeutic monoclonal anti-PD-1 antibody with high binding affinity to PD-1 and enhanced potency to activate human T cells. Cancer immunology immunotherapy: CII. (2024) 73:60. doi: 10.1007/s00262-024-03635-3
39
HaanenJBAGCarbonnelFRobertCKerrKMPetersSLarkinJet al. Management of toxicities from immunotherapy: ESMO clinical practice guidelines for diagnosis, treatment and follow-up. Ann Oncol. (2017) 28:i119–42. doi: 10.1093/annonc/mdy162
40
SunYHuangJHuFXueRChangXChengLet al. Expert Committee of Multi-disciplinary expert consensus on cutaneous adverse events caused by immune checkpoint inhibitors. Multi-disciplinary expert consensus on cutaneous adverse events caused by immune checkpoint inhibitors. Chin J Clin Med. (2025) 32:1–16. doi: 10.12025/j.issn.1008-6358.2025.20250020
41
Clinical practice guideline: immune checkpoint inhibitor toxicity management. Cancer Care Ontario. (2018).
42
MenterAGelfandJMConnorCArmstrongAWCordoroKMDavisDMRet al. Joint American Academy of Dermatology-National Psoriasis Foundation guidelines of care for the management of psoriasis with systemic nonbiologic therapies. J Am Acad Dermatol. (2020) 82:1445–86. doi: 10.1016/j.jaad.2020.02.044
Summary
Keywords
toripalimab, esophageal cancer, psoriasis, case report, adverse effects
Citation
Zhao L, Cheng Z and Li P (2025) Toripalimab induces exacerbation of psoriasis in an esophageal cancer patient: a case report. Front. Oncol. 15:1596818. doi: 10.3389/fonc.2025.1596818
Received
20 March 2025
Accepted
11 August 2025
Published
27 August 2025
Volume
15 - 2025
Edited by
Khalil Saleh, Gustave Roussy Cancer Campus, France
Reviewed by
Mohsen Khosravi, Zahedan University of Medical Sciences, Iran
Meng Wu, Shandong University, China
Updates
Copyright
© 2025 Zhao, Cheng and Li.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Luping Zhao, lilyluping@126.com
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.