TNFRSF14, encoding the receptor HVEM, is frequently mutated in germinal center (GC)-derived B cell lymphomas. In this issue, Mintz et al. demonstrate that the HVEM-BTLA axis restrains T cell help to GC B cells. Mutation-associated loss of this interaction promotes B cell proliferation through exaggerated T cell help, explaining how HVEM loss contributes to GC lymphomagenesis and revealing a cell-extrinsic tumor-suppressor role for BTLA.

中文翻译：

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萌发中心的AT细胞B细胞肿瘤抑制轴

编码受体HVEM的TNFRSF14在生发中心（GC）衍生的B细胞淋巴瘤中经常发生突变。在本期中，Mintz等人。证明HVEM-BTLA轴抑制了T细胞对GC B细胞的帮助。突变相关的这种相互作用的丧失通过夸张的T细胞帮助促进了B细胞的增殖，从而解释了HVEM丧失如何促进GC淋巴瘤的发生，并揭示了BTLA的细胞外源性肿瘤抑制作用。