Journal of hematopathology · 2026
EBV-positive Hodgkin lymphoma with an immunosuppressive microenvironment during guselkumab (interleukin-23 inhibitor) therapy for chronic plaque psoriasis.
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Shah Bhaumik, Franco-Barraza Janusz, Cai Kathy Q, Dmitrieva Mariia, Messmer Marcus, Yang Yibin, Wasik Mariusz, Cukierman Edna, Nejati Reza
Аннотация
BACKGROUND: Psoriasis is an independent risk factor for classic Hodgkin lymphoma (cHL). Guselkumab has a favorable malignancy safety profile in clinical trials.
PURPOSE: To report the first documented Epstein-Barr virus (EBV)-positive cHL arising in a biologic-naive patient with psoriatic arthritis during guselkumab therapy for chronic plaque psoriasis, and to describe its tumor microenvironment.
METHODS: Excisional biopsy with immunohistochemistry, EBER in situ hybridization, and targeted sequencing, plus spatial single-cell proteomics (9-plex sequential immunofluorescence) of the diagnostic lymph node.
RESULTS: A man in his early 40s developed night sweats, syncope, and bulky right cervical lymphadenopathy 7 months after starting guselkumab. Biopsy showed mixed-cellularity EBV-positive cHL (latency IIa: EBER+, LMP1+, EBNA-2-). HRS cells were weak PAX5+, CD20 negative, CD15+, strong CD30+, OCT2 negative/weak, BOB1 negative/weak, and strong CD200+. The microenvironment contained CTLA4+ immunosuppressive T cells (10.15%), M2 macrophages (10.35%), modest Th2 cells (0.38%), a low Th1/Th2 ratio (~0.39), and Th17 cells (~13%). GATA3 and CCR4 immunohistochemistry confirmed modest Th2 skewing. After guselkumab was stopped, he achieved a complete metabolic response with ABVD and involved-site radiotherapy and remains in remission on apremilast.
CONCLUSIONS: The short latency and atypical Th2-skewed, myeloid-enriched microenvironment, in contrast to the typical Th1-dominant profile of EBV-positive cHL, raise the possibility of immune-milieu alteration under IL-23 inhibition. This case supports continued pharmacovigilance for rare lymphomas in patients receiving IL-23 inhibitors and the need for larger studies to clarify potential class effects.
PURPOSE: To report the first documented Epstein-Barr virus (EBV)-positive cHL arising in a biologic-naive patient with psoriatic arthritis during guselkumab therapy for chronic plaque psoriasis, and to describe its tumor microenvironment.
METHODS: Excisional biopsy with immunohistochemistry, EBER in situ hybridization, and targeted sequencing, plus spatial single-cell proteomics (9-plex sequential immunofluorescence) of the diagnostic lymph node.
RESULTS: A man in his early 40s developed night sweats, syncope, and bulky right cervical lymphadenopathy 7 months after starting guselkumab. Biopsy showed mixed-cellularity EBV-positive cHL (latency IIa: EBER+, LMP1+, EBNA-2-). HRS cells were weak PAX5+, CD20 negative, CD15+, strong CD30+, OCT2 negative/weak, BOB1 negative/weak, and strong CD200+. The microenvironment contained CTLA4+ immunosuppressive T cells (10.15%), M2 macrophages (10.35%), modest Th2 cells (0.38%), a low Th1/Th2 ratio (~0.39), and Th17 cells (~13%). GATA3 and CCR4 immunohistochemistry confirmed modest Th2 skewing. After guselkumab was stopped, he achieved a complete metabolic response with ABVD and involved-site radiotherapy and remains in remission on apremilast.
CONCLUSIONS: The short latency and atypical Th2-skewed, myeloid-enriched microenvironment, in contrast to the typical Th1-dominant profile of EBV-positive cHL, raise the possibility of immune-milieu alteration under IL-23 inhibition. This case supports continued pharmacovigilance for rare lymphomas in patients receiving IL-23 inhibitors and the need for larger studies to clarify potential class effects.