Abstract：
Nodal peripheral T-cell lymphoma (PTCL) is a heterogeneous category including angioimmunoblastic T-cell lymphoma (AITL), PTCL of follicular helper T-cell (Tfh) phenotype (PTCL-Tfh), and PTCL, not otherwise specified (PTCL-NOS). We explored Tfh marker profiles in nodal PTCL. Nodal PTCLs (n = 129) were reclassified into AITL (58%; 75/129), PTCL-Tfh (26%; 34/129), and PTCL-NOS (16%; 20/129). Histologically, clear cell clusters, high endothelial venules, follicular dendritic cell proliferation, EBV+ cells, and Hodgkin-Reed-Sternberg (HRS)-like cells were more common in AITL than PTCL-Tfh (HRS-like cells, P = .005; otherwise, P < .001) and PTCL-NOS (HRS-like cells, P = .028; otherwise, P < .001). PTCL-NOS had a higher Ki-67 index than AITL (P = .001) and PTCL-Tfh (P = .002). Clinically, AITL had frequent B symptoms (versus PTCL-Tfh, P = .010), while PTCL-NOS exhibited low stage (versus AITL + PTCL-Tfh, P = .036). Positive Tfh markers were greater in AITL (3.5 ± 1.1) than PTCL-Tfh (2.9 ± 0.9; P = .006) and PTCL-NOS (0.5 ± 0.5; P < .001). Tfh markers showed close correlations among them and AITL-defining histology. By clustering analysis, AITL and PTCL-NOS were relatively exclusively clustered, while PTCL-Tfh overlapped with them. Survival was not different among the PTCL entities. By Cox regression, sex and ECOG performance status (PS) independently predicted shorter progression-free survival in the whole cohort (male, P = .001, HR = 2.5; PS ≥ 2, P = .010, HR = 1.9) and in \'Tfh-lymphomas\' (ie, AITL + PTCL-Tfh) (male, P = .001, HR = 2.6; PS ≥ 2, P = .016, HR = 2.1), while only PS predicted shorter overall survival (OS) in the whole cohort (P = .012, HR = 2.7) and in \'Tfh-lymphomas\' (P = .001; HR = 3.2). ICOS predicted favorable OS in \'Tfh-lymphomas\' (log-rank; P = .016). Despite the overlapping features, nodal PTCL entities could be characterized by Tfh markers revealing clinicopathologic implications.
摘要：
淋巴结外周T细胞淋巴瘤(PTCL)是一个异质性类别,包括血管免疫母细胞性T细胞淋巴瘤(AITL),滤泡辅助性T细胞（Tfh）表型（PTCL-Tfh）的PTCL，和PTCL,没有另外规定(PTCL-NOS)。我们探索了节点PTCL中的Tfh标记谱。节点PTCL（n=129）被重新分类为AITL[58％；75/129]，PTCL-Tfh[26%;34/129]和PTCL-NOS[16%;20/129]。组织学上,透明细胞簇，高内皮小静脉,滤泡树突状细胞增殖，EBV+细胞和霍奇金-里德-斯特恩伯格（HRS）样细胞在AITL中比PTCL-Tfh更常见（HRS样细胞，p=0.005；否则，p<0.001)和PTCL-NOS(HRS样细胞，p=0.028；否则，p<0.001)。PTCL-NOS的Ki-67指数高于AITL(p=0.001)和PTCL-Tfh(p=0.002)。临床上,AITL经常出现B症状（与PTCL-Tfh,p=0.010),而PTCL-NOS表现为低阶段(vs.AITL+PTCL-Tfh,p=0.036)。AITL（3.5±1.1）中的Tfh阳性标志物高于PTCL-Tfh（2.9±0.9；p=0.006）和PTCL-NOS（0.5±0.5；p<0.001）。Tfh标记物之间显示出与AITL定义的组织学密切相关。通过聚类分析，AITL和PTCL-NOS相对完全聚集，而PTCL-Tfh与它们重叠。PTCL实体之间的生存率没有差异。通过Cox回归，性别和ECOG表现状态（PS）独立预测了整个队列中更短的无进展生存期（男性，p=rmfl0.001，HR=2.5；PS≥2，p=0.010，HR=1.9）和“Tfh淋巴瘤”（即，AITL+PTCL-Tfh)(男,p=0.001，HR=2.6；PS≥2，p=0.016，HR=2.1），而仅PS预测整个队列（p=0.012，HR=2.7）和Tfh淋巴瘤（p=0.001；HR=3.2）的总生存期（OS）较短。ICOS预测了“Tfh淋巴瘤”的有利OS(对数秩；p=0.016)。尽管功能重叠，淋巴结PTCL实体可以通过Tfh标记来表征，从而揭示临床病理意义。
