决定异体 CAR T 细胞排斥与扩增的细胞和分子机制
Cellular and molecular mechanisms determining allogeneic CAR T cell rejection and expansion.
我们评估了11例接受单一批次cemacabtagene ansegedleucel(cema-cel)治疗的大B细胞淋巴瘤患者,cemacabtagene ansegedleucel是一种异体抗CD19 CAR T产品。
英文原题:Latent Neoehrlichia mikurensis Infections May Be Reactivated in Patients With B-Cell Lymphomas Treated With Rituximab.
我们通过测定N.的发病率来验证这一假设。
细胞内、蜱传的Neoehrlichia(N.)mikurensis可在B细胞防御受损的患者中引起neoehrlichiosis,而免疫正常个体常为该感染的健康携带者。我们假设N. mikurensis诱导潜伏感染,并在B细胞免疫受损时再激活。我们通过测定97例接受抗CD20抗体治疗(rituximab)的B细胞淋巴瘤患者中N. mikurensis再激活的发生率,并评估潜伏感染个体中是否存在N. mikurensis特异性T细胞,来检验这一假设。4例患者(4%)出现N. mikurensis感染再激活,4例患者(4%)在开始B细胞抑制前有无症状感染。所有8例感染N. mikurensis的患者均具有N. mikurensis特异性、表达穿孔素的Th1和CD8+ T细胞群,并伴有CXCL10和IFN-γ上调,而未感染的淋巴瘤患者缺乏这些T细胞亚群。感染的淋巴瘤患者还具有扩增的γδ T细胞群。本研究支持存在潜伏、可再激活的N. mikurensis感染这一观点。
The intracellular, tick-borne bacterium Neoehrlichia (N.) mikurensis can cause neoehrlichiosis in patients with compromised B-cell defences, while immunocompetent individuals are frequently healthy carriers of the infection. We hypothesised that N. mikurensis induces latent infections that reactivate when B-cell immunity is compromised. We tested this hypothesis by determining the incidence of N. mikurensis reactivation in 97 patients with B-cell lymphomas who were treated with anti-CD20 antibody therapy (rituximab) and evaluating the presence of N. mikurensis-specific T cells in latently infected individuals. Four patients (4%) reactivated N. mikurensis infection and four patients (4%) had asymptomatic infection before the initiation of B-cell suppression. All eight patients who were infected with N. mikurensis had N. mikurensis-specific, perforin-expressing Th1 and CD8+ T-cell populations with up-regulation of CXCL10 and IFN-γ, in contrast to the noninfected lymphoma patients who lacked these T-cell subsets. The infected lymphoma patients also had expanded γδ T-cell populations. This study supports the notion of latent, reactivatable N. mikurensis infections.
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