Reduced expression of programmed cell death 1 and programmed cell death ligand 1 in infiltrating inflammatory cells of lichen planus without administration of immune checkpoint inhibitors

Kazufumi, Shirouchi; Koshikawa, Sachiko; Shinya, Koichiro; Watanabe, Hideaki; Izumi, Mitsuru; Yoshimura, Kiyoshi; Sueki, Hirohiko

doi:10.1111/1346-8138.15977

Cited by 3 publications

(5 citation statements)

References 14 publications

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“…In support of the present study, it has been shown that PD-1 and PD-L1 expression levels were minimal in 12 patients with LP compared to 12 patients with erythema multiforme in a study done by Shirouchi et al [ 25 ]. Moreover, Costa et al [ 4 ] reported reduced/absent expression of PD-L1 with lower levels of PD-1 + T-lymphocyte cells in the OLP patients.…”

Section: Discussionsupporting

confidence: 89%

“…Based on the fact that PD-1/PD-L1 interaction inhibits lymphocyte activation, the study results support the hypothesis that decreased expression of PD-1 and PD-L1 in LP patients could accelerate lymphocyte infiltration and cause failure to regulate CD8 + T-lymphocytes targeting the epidermis in the pathogenesis of LP and also low PD-L1 expression may accelerate macrophage infiltration [ 25 ].…”

Section: Discussionsupporting

confidence: 71%

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Assessment of PD-1 and PD-L1 tissue expression levels in lichen planus patients: a case–control study

Elmasry,

Mosaad,

Azzam

et al. 2024

Arch Dermatol Res

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Programmed cell death protein-1 (PD-1) is an immune checkpoint protein, PD-1 interaction with PD ligand-1 (PD-L1) is essential for maintaining immunological tolerance. The study aimed to study and compare the levels of PD-1 and PD-L1 in lesional and nonlesional skin of lichen planus (LP) patients and compare these levels to normal healthy controls to assess their role in the pathogenesis of LP. This case–control study involved 30 patients with LP and 30 healthy age-and sex-matched controls. After clinical assessment of the severity by LP severity index score (LPSI), skin biopsies were taken from lesional and nonlesional skin of LP patients and from normal skin in healthy controls for assessment of the tissue levels of PD-1 and PD-L1 by ELISA. The tissue levels of both PD-1 and PD-L1 were significantly higher in healthy controls than in both lesional and nonlesional skin of LP patients (P < 0.001). Also, significantly higher PD-l and PD-L1 levels in nonlesional skin than in lesional skin of LP patients were reported (P < 0.001). No significant correlations were found between lesional and nonlesional PD-1, PD-L1 levels, or LPSI score. Based on the fact that PD-1/PD-L1 interaction is important to maintain tolerance and protection against autoimmune diseases, in addition to our study results that revealed lower levels of PD-1/PD-L1 in LP skin than in healthy skin, we can conclude that PD-1/PDL-1 may be incriminated in the pathogenesis of LP. ClinicalTrials.govID: NCT04892381.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionsupporting

confidence: 71%

Assessment of PD-1 and PD-L1 tissue expression levels in lichen planus patients: a case–control study

Elmasry,

Mosaad,

Azzam

et al. 2024

Arch Dermatol Res

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“…Finally, numerous papers [ 214 , 215 , 216 ] report that the PD-L1 protein overexpressed in the membrane of tumor cells can induce apoptosis in T lymphocytes, thus eliminating the antitumor response. This mechanism could operate early in OLP as well [ 217 , 218 , 219 , 220 , 221 ].…”

Section: Discussionmentioning

confidence: 99%

Hallmarks of Cancer Expression in Oral Lichen Planus: A Scoping Review of Systematic Reviews and Meta-Analyses

González‐Moles

Pino

Ramos‐García

2022

IJMS

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Oral lichen planus (OLP) is a common chronic inflammatory disease of unknown etiology and likely autoimmune nature that is currently considered an oral potentially malignant disorder, implying that patients suffering from this process are at risk of developing oral cancer in their lifetime. The molecular alterations that develop in OLP and that make the affected oral epithelium predisposed to malignancy are unknown, although, as in other autoimmune diseases (ulcerative colitis, primary biliary cirrhosis, etc.), they may be linked to oncogenesis-promoting effects mediated by the inflammatory infiltrate. So far there is no in-depth knowledge on how these hallmarks of cancer are established in the cells of the oral epithelium affected by OLP. In this scoping review of systematic reviews and meta-analyses the state of evidence based knowledge in this field is presented, to point out gaps of evidence and to indicate future lines of research. MEDLINE, Embase, Cochrane Library and Dare were searched for secondary-level studies published before October 2022. The results identified 20 systematic reviews and meta-analyses critically appraising the hallmarks tumor-promoting inflammation (n = 17, 85%), sustaining proliferative signaling (n = 2, 10%), and evading growth suppressors (n = 1, 5%). No evidence was found for the other hallmarks of cancer in OLP. In conclusion, OLP malignization hypothetically derives from the aggressions of the inflammatory infiltrate and a particular type of epithelial response based on increased epithelial proliferation, evasion of growth-suppressive signals and lack of apoptosis. Future evidence-based research is required to support this hypothesis.

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“…48 Interestingly, expression of PD-1 and PD-L1, which is believed to lead to increased infiltration of lymphocytes and possibly macrophages in the epidermis, was found to be reduced in de novo lichen planus (LP) compared with erythema multiforme lesions, and potentially contributes to development of LP. 49 Psoriasis is characterized by increased keratinocyte proliferation, resulting in well-demarcated, scaly, erythematous plaques. 22 ICI-induced psoriasis accounts for approximately 4% of all cutaneous irAEs, 50 and development of guttate psoriasis or psoriasis involving > 10% of body surface area (BSA) has been found to be predictive of a good response to ICI therapy.…”

Section: Inflammatorymentioning

confidence: 99%

“…Cutaneous pathogens in the skin microbiome may lead to increased activation of the innate immune system, which in turn generates a Th1 response resulting in ICI‐associated lichenoid reactions 48 . Interestingly, expression of PD‐1 and PD‐L1, which is believed to lead to increased infiltration of lymphocytes and possibly macrophages in the epidermis, was found to be reduced in de novo lichen planus (LP) compared with erythema multiforme lesions, and potentially contributes to development of LP 49 …”

Section: Mechanisms Of Cutaneous Immune‐related Adverse Eventsmentioning

confidence: 99%

Mechanisms of dermatological toxicities to immune checkpoint inhibitor cancer therapies

Seervai

Sinha

Kulkarni

2022

Clinical and Experimental Dermatology

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The discovery of immune checkpoint inhibition (ICI) sparked a revolution in the era of targeted anticancer therapy. However, although monoclonal antibodies targeting the cytotoxic T-lymphocyte antigen-4 and programmed death-1 axes have improved survival in patients with advanced cancers, these immunotherapies are associated with a wide spectrum of dermatological immune-related adverse events (irAEs), ranging from mild to life-threatening. Several publications have addressed the clinical and histopathological classification of these skin-directed irAEs, their impact on anti-tumour immunity and survival, and the critical role of supportive oncological dermatology in their management. In this paper, we review the current understanding of the mechanistic drivers of immune-related skin toxicities with a focus on inflammatory, immunobullous and melanocyte/pigment-related reactions. We detail the specific immune-based mechanisms that may underlie different cutaneous reactions. We also discuss potential mechanisms as they relate to extracutaneous irAEs and the lessons learned from these, the potential overlap with cutaneous irAEs, techniques to study differences in immune-related vs. de novo skin reactions, and how treatment of these AEs impacts cancer treatment, patient quality of life and overall survival. An improved understanding of the mechanistic basis of cutaneous irAEs will allow clinicians to develop and use blood-based biomarkers that could help ultimately predict onset and/or severity of these irAEs, and to implement rational mechanistic-based treatment strategies that are targeted to the irAEs while potentially avoiding reducing the anti-tumour effect of ICIs.

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Reduced expression of programmed cell death 1 and programmed cell death ligand 1 in infiltrating inflammatory cells of lichen planus without administration of immune checkpoint inhibitors

Cited by 3 publications

References 14 publications

Assessment of PD-1 and PD-L1 tissue expression levels in lichen planus patients: a case–control study

Assessment of PD-1 and PD-L1 tissue expression levels in lichen planus patients: a case–control study

Hallmarks of Cancer Expression in Oral Lichen Planus: A Scoping Review of Systematic Reviews and Meta-Analyses

Mechanisms of dermatological toxicities to immune checkpoint inhibitor cancer therapies

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