Division of Hematology/Oncology, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, United States of America.
UCLA AIDS Institute and the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, David Geffen School of Medicine at UCLA, Los Angeles, California, United States of America.
PLoS Pathog. 2021 Apr 1;17(4):e1009404. doi: 10.1371/journal.ppat.1009404. eCollection 2021 Apr.
Due to the durability and persistence of reservoirs of HIV-1-infected cells, combination antiretroviral therapy (ART) is insufficient in eradicating infection. Achieving HIV-1 cure or sustained remission without ART treatment will require the enhanced and persistent effective antiviral immune responses. Chimeric Antigen Receptor (CAR) T-cells have emerged as a powerful immunotherapy and show promise in treating HIV-1 infection. Persistence, trafficking, and maintenance of function remain to be a challenge in many of these approaches, which are based on peripheral T cell modification. To overcome many of these issues, we have previously demonstrated successful long-term engraftment and production of anti-HIV CAR T cells in modified hematopoietic stem cells (HSCs) in vivo. Here we report the development and in vivo testing of second generation CD4-based CARs (CD4CAR) against HIV-1 infection using a HSCs-based approach. We found that a modified, truncated CD4-based CAR (D1D2CAR) allows better CAR-T cell differentiation from gene modified HSCs, and maintains similar CTL activity as compared to the full length CD4-based CAR. In addition, D1D2CAR does not mediate HIV infection or stimulation mediated by IL-16, suggesting lower risk of off-target effects. Interestingly, stimulatory domains of 4-1BB but not CD28 allowed successful hematopoietic differentiation and improved anti-viral function of CAR T cells from CAR modified HSCs. Addition of 4-1BB to CD4 based CARs led to faster suppression of viremia during early untreated HIV-1 infection. D1D2CAR 4-1BB mice had faster viral suppression in combination with ART and better persistence of CAR T cells during ART. In summary, our data indicate that the D1D2CAR-41BB is a superior CAR, showing better HSC differentiation, viral suppression and persistence, and less deleterious functions compared to the original CD4CAR, and should continue to be pursued as a candidate for clinical study.
由于 HIV-1 感染细胞的持久性和持续性,联合抗逆转录病毒疗法(ART)不足以消除感染。要实现 HIV-1 的治愈或持续缓解而不进行 ART 治疗,将需要增强和持续有效的抗病毒免疫反应。嵌合抗原受体(CAR)T 细胞已成为一种强大的免疫疗法,在治疗 HIV-1 感染方面显示出前景。在许多基于外周 T 细胞修饰的方法中,持久性、迁移和功能维持仍然是一个挑战。为了克服许多这些问题,我们之前已经证明,在体内对修饰的造血干细胞(HSCs)进行修饰后,可以成功地长期植入和产生抗 HIV 的 CAR T 细胞。在这里,我们报告了使用基于 HSCs 的方法开发和体内测试针对 HIV-1 感染的第二代基于 CD4 的 CAR(CD4CAR)。我们发现,一种修饰的、截断的基于 CD4 的 CAR(D1D2CAR)可以更好地从基因修饰的 HSCs 中分化出 CAR-T 细胞,并保持与全长基于 CD4 的 CAR 相似的 CTL 活性。此外,D1D2CAR 不会介导 HIV 感染或由 IL-16 介导的刺激,表明其脱靶效应的风险较低。有趣的是,4-1BB 的刺激结构域而不是 CD28 的刺激结构域允许 CAR 修饰的 HSCs 中的 CAR-T 细胞成功进行造血分化并改善抗病毒功能。在基于 CD4 的 CAR 上添加 4-1BB 可导致在未经治疗的 HIV-1 感染早期更快地抑制病毒血症。在与 ART 联合使用时,D1D2CAR-41BB 小鼠更快地抑制病毒,并且在 ART 期间 CAR-T 细胞的持续时间更长。总之,我们的数据表明,与原始的 CD4CAR 相比,D1D2CAR-41BB 是一种优越的 CAR,显示出更好的 HSC 分化、病毒抑制和持久性,以及更少的有害功能,应该继续作为临床研究的候选物进行探索。