Department of Immunoregulation and Immunodiagnostics, Chittaranjan National Cancer Institute (CNCI), Kolkata, India.
PLoS One. 2013;8(1):e47434. doi: 10.1371/journal.pone.0047434. Epub 2013 Jan 11.
In spite of sufficient data on Neem Leaf Glycoprotein (NLGP) as a prophylactic vaccine, little knowledge currently exists to support the use of NLGP as a therapeutic vaccine. Treatment of mice bearing established sarcomas with NLGP (25 µg/mice/week subcutaneously for 4 weeks) resulted in tumor regression or dormancy (Tumor free/Regressor, 13/24 (NLGP), 4/24 (PBS)). Evaluation of CD8(+) T cell status in blood, spleen, TDLN, VDLN and tumor revealed increase in cellular number. Elevated expression of CD69, CD44 and Ki67 on CD8(+) T cells revealed their state of activation and proliferation by NLGP. Depletion of CD8(+) T cells in mice at the time of NLGP treatment resulted in partial termination of tumor regression. An expansion of CXCR3(+) and CCR5(+) T cells was observed in the TDLN and tumor, along with their corresponding ligands. NLGP treatment enhances type 1 polarized T-bet expressing T cells with downregulation of GATA3. Treg cell population was almost unchanged. However, T∶Treg ratios significantly increased with NLGP. Enhanced secretion/expression of IFNγ was noted after NLGP therapy. In vitro culture of T cells with IL-2 and sarcoma antigen resulted in significant enhancement in cytotoxic efficacy. Consistently higher expression of CD107a was also observed in CD8(+) T cells from tumors. Reinoculation of sarcoma cells in tumor regressed NLGP-treated mice maintained tumor free status in majority. This is correlated with the increment of CD44(hi)CD62L(hi) central memory T cells. Collectively, these findings support a paradigm in which NLGP dynamically orchestrates the activation, expansion, and recruitment of CD8(+) T cells into established tumors to operate significant tumor cell lysis.
尽管有足够的数据表明印苦楝叶糖蛋白(NLGP)可作为预防性疫苗,但目前对于将 NLGP 作为治疗性疫苗的应用知之甚少。用 NLGP(每周 25 µg/小鼠,皮下注射 4 周)治疗已建立的肉瘤小鼠,导致肿瘤消退或休眠(无肿瘤/消退者,NLGP 为 13/24,PBS 为 4/24)。在血液、脾脏、TDLN、VDLN 和肿瘤中评估 CD8+T 细胞状态时,发现细胞数量增加。NLGP 上调 CD8+T 细胞上的 CD69、CD44 和 Ki67 的表达,表明其处于激活和增殖状态。在 NLGP 治疗时耗尽小鼠中的 CD8+T 细胞,导致肿瘤消退部分终止。在 TDLN 和肿瘤中观察到 CXCR3+和 CCR5+T 细胞的扩张,以及它们相应的配体。NLGP 治疗增强了表达 1 型极化 T-bet 的 T 细胞,下调 GATA3。Treg 细胞群几乎没有变化。然而,NLGP 治疗后 T∶Treg 比值显著增加。治疗后注意到 IFNγ 的分泌/表达增强。用 IL-2 和肉瘤抗原体外培养 T 细胞可显著增强细胞毒性效力。在来自肿瘤的 CD8+T 细胞中也观察到 CD107a 的表达明显增强。在肿瘤消退的 NLGP 治疗小鼠中重新接种肉瘤细胞,使大多数小鼠保持无肿瘤状态。这与 CD44(高)CD62L(高)中央记忆 T 细胞的增加有关。综上所述,这些发现支持一种范式,即 NLGP 动态协调 CD8+T 细胞在已建立的肿瘤中的激活、扩增和募集,以实现显著的肿瘤细胞裂解。