![An 82-year-old man presented with cervical and axillar lymphadenopathy without symptoms. Cervical lymph node biopsy showed a vague nodular structure (panel A: original magnification ×20 [inset ×200], hematoxylin and eosin [H&E] stain; and panel B: original magnification ×20, immunohistochemistry for immunoglobulin D) with aggregation of atypical lymphoid cells with clear cytoplasm expressing CD3 (panel C: original magnification ×200), CD10, BCL6, and PD-1 (panel C inset: original magnification ×200). Sinuses were partially occupied by large lymphoid cells with anaplastic morphology (panel D: original magnification ×200 [inset ×400], H&E stain). The cells were positive for CD20, CD79a, PAX5, CD30 (panel E: original magnification ×100), Epstein-Barr virus (EBV) LMP1, and EBV-encoded small nuclear early region in situ hybridization (panel F: original magnification ×100) and negative for pan–T-cell markers, CD15, and ALK. Clonality assessment showed monoclonal T cells and polyclonal B cells. A diagnosis of follicular T-cell lymphoma was made. / EBV+ B cells, sometimes recognized in peripheral T-cell lymphoma (PTCL), are usually admixed with neoplastic T cells. This suggests abnormal local immune status induced by lymphoma cells. In this case, virtually all EBV-infected B cells were confined to the sinuses. This distribution pattern, mimicking anaplastic large-cell lymphoma, expands the spectrum of B-cell proliferation observed in PTCL. The precise mechanism of the “intrasinusal expansion pattern” is as-yet unknown, but some adhesion molecules of endothelial cells and lymphoma cells may contribute as discussed in intravascular lymphoma. Detailed phenotypic analysis including EBV leads to accurate understanding of pathogenesis.](https://ash.silverchair-cdn.com/ash/content_public/journal/blood/129/13/10.1182_blood-2016-11-751974/4/m_blood751974f1.jpeg?Expires=1734533446&Signature=x6aWiV5r1FIZcH7L8lvxwfDWedrS1LRVYkzIs43Z8fnY8IuxJtZE8VuNwBLjaiZ6JYe55tFUMAC4hi6jBPIs5Hn7UfZVtokqrqRNAtIDB2Bum9Fm~851sNTpF-9XxawcBGsqiMzShYZfGlcRcYHXR98h5UGveYfTkw2WWjsQOEDTv8ucGIsnE7ztcPOhBlwgKGDtUPbpr4rBXS6gNj0GXGlk7Th-IQVcspIB1hkStfrciUqHIHY5YVAjix0NLqPdJ03ogaurLwRRt5TGLlKOGXwhLiixJTXcPiMoVUhSEWPwNXOSLbAClcVNjxXi4r3e58gKqNqGMqMbzgmfTo4d-A__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
An 82-year-old man presented with cervical and axillar lymphadenopathy without symptoms. Cervical lymph node biopsy showed a vague nodular structure (panel A: original magnification ×20 [inset ×200], hematoxylin and eosin [H&E] stain; and panel B: original magnification ×20, immunohistochemistry for immunoglobulin D) with aggregation of atypical lymphoid cells with clear cytoplasm expressing CD3 (panel C: original magnification ×200), CD10, BCL6, and PD-1 (panel C inset: original magnification ×200). Sinuses were partially occupied by large lymphoid cells with anaplastic morphology (panel D: original magnification ×200 [inset ×400], H&E stain). The cells were positive for CD20, CD79a, PAX5, CD30 (panel E: original magnification ×100), Epstein-Barr virus (EBV) LMP1, and EBV-encoded small nuclear early region in situ hybridization (panel F: original magnification ×100) and negative for pan–T-cell markers, CD15, and ALK. Clonality assessment showed monoclonal T cells and polyclonal B cells. A diagnosis of follicular T-cell lymphoma was made.
EBV+ B cells, sometimes recognized in peripheral T-cell lymphoma (PTCL), are usually admixed with neoplastic T cells. This suggests abnormal local immune status induced by lymphoma cells. In this case, virtually all EBV-infected B cells were confined to the sinuses. This distribution pattern, mimicking anaplastic large-cell lymphoma, expands the spectrum of B-cell proliferation observed in PTCL. The precise mechanism of the “intrasinusal expansion pattern” is as-yet unknown, but some adhesion molecules of endothelial cells and lymphoma cells may contribute as discussed in intravascular lymphoma. Detailed phenotypic analysis including EBV leads to accurate understanding of pathogenesis.
An 82-year-old man presented with cervical and axillar lymphadenopathy without symptoms. Cervical lymph node biopsy showed a vague nodular structure (panel A: original magnification ×20 [inset ×200], hematoxylin and eosin [H&E] stain; and panel B: original magnification ×20, immunohistochemistry for immunoglobulin D) with aggregation of atypical lymphoid cells with clear cytoplasm expressing CD3 (panel C: original magnification ×200), CD10, BCL6, and PD-1 (panel C inset: original magnification ×200). Sinuses were partially occupied by large lymphoid cells with anaplastic morphology (panel D: original magnification ×200 [inset ×400], H&E stain). The cells were positive for CD20, CD79a, PAX5, CD30 (panel E: original magnification ×100), Epstein-Barr virus (EBV) LMP1, and EBV-encoded small nuclear early region in situ hybridization (panel F: original magnification ×100) and negative for pan–T-cell markers, CD15, and ALK. Clonality assessment showed monoclonal T cells and polyclonal B cells. A diagnosis of follicular T-cell lymphoma was made.
EBV+ B cells, sometimes recognized in peripheral T-cell lymphoma (PTCL), are usually admixed with neoplastic T cells. This suggests abnormal local immune status induced by lymphoma cells. In this case, virtually all EBV-infected B cells were confined to the sinuses. This distribution pattern, mimicking anaplastic large-cell lymphoma, expands the spectrum of B-cell proliferation observed in PTCL. The precise mechanism of the “intrasinusal expansion pattern” is as-yet unknown, but some adhesion molecules of endothelial cells and lymphoma cells may contribute as discussed in intravascular lymphoma. Detailed phenotypic analysis including EBV leads to accurate understanding of pathogenesis.
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