CAR-T（CAR-T）细胞疗法在非肿瘤性疾病中的应用
Chimeric antigen receptor T (CAR-T) cell therapy in non-oncological diseases.
CAR-T（CAR-T）细胞在血液系统恶性肿瘤中的应用推动了这种免疫治疗形式的显著进展。
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
煽风点火：IFN-γ 助推 CAR-T 炎症和血细胞减少
英文原题：Fanning the flames: IFN-γ fuels CAR-T inflammation and cytopenia.
查看英文原题
Fanning the flames: IFN-γ fuels CAR-T inflammation and cytopenia.
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中文摘要
CAR-T 细胞疗法已改变血液系统恶性肿瘤治疗，但严重炎症毒性仍限制其更广泛应用。本期JCI中，Goala等揭示了IFN-γ驱动炎症与中性粒细胞稳态紊乱之间的机制联系，指出细胞因子释放综合征（CRS）和免疫细胞相关血液学毒性（ICAHT）源自共同的生物学通路。研究利用IL-2Rα缺陷小鼠和患者样本，发现IFN-γ抑制IL-17A和粒细胞集落刺激因子（G-CSF），从而扰乱粒细胞生成并降低中性粒细胞存活。值得注意的是，阻断IFN-γ可同时减轻CRS和中性粒细胞减少，且不削弱CAR-T 疗效，提示这可能成为开发更安全、耐受性更佳细胞疗法的途径。
展开英文摘要原文
Chimeric antigen receptor T cell (CAR-T) therapy has transformed the treatment of hematologic malignancies, yet, severe inflammatory toxicities continue to limit its broader use. In this issue of the JCI, Goala et al. uncovered a mechanistic link between IFN- -driven inflammation and disrupted neutrophil homeostasis, revealing that cytokine release syndrome (CRS) and immune cell-associated hematologic toxicity (ICAHT) stem from a shared biological pathway.
Using IL-2Ra-deficient mice and patient samples, they showed that IFN- suppressed IL-17A and granulocyte colony-stimulating factor (G-CSF), disrupting granulopoiesis and neutrophil survival. Strikingly, IFN- blockade eased both CRS and neutropenia without diminishing CAR-T efficacy, suggesting a path toward safer, better-tolerated cell therapies.
论文信息
- 作者
- Bailey SR、Maus MV
- 第一作者单位
- Division of Pediatric Hematology/Oncology, Department of Pediatrics, Department of Microbiology, Immunology and Cancer Biology, University of Virginia, Charlottesville, Virginia, USA.United States
- 通讯作者单位
- Cellular Immunotherapy Program, Mass General Cancer Center, Krantz Family Center for Cancer Research, Massachusetts General Hospital, Department of Medicine, Harvard Medical School, Boston, Masschusetts, USA.United States
- 文献类型
- 美国政府（非公共卫生署）资助研究
- 期刊
- The Journal of clinical investigation2026 Jan 2
- 原文标识
- PubMed 41480762 · DOI 10.1172/JCI201161
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