Ankrom Emily, Dalesandro Brianna, Pires Marcos M, Thévenin Damien
Department of Chemistry, Lehigh University, Bethlehem, Pennsylvania, 18015, USA.
Department of Chemistry, University of Virginia, Charlottesville, Virginia, 22904, USA.
ChemMedChem. 2024 Dec 2;19(23):e202400356. doi: 10.1002/cmdc.202400356. Epub 2024 Oct 26.
Many current cancer immunotherapies function by redirecting immune system components to recognize cancer biomarkers and initiate a cytotoxic attack. The lack of a universal tumor biomarker limits the therapeutic potential of these approaches. However, one feature characteristic of nearly all solid tumors is extracellular acidity. This inherent acidity provides the basis for targeted drug delivery via the pH-low insertion peptide (pHLIP), which selectively accumulates in tumors in vivo due to a pH-dependent membrane insertion propensity. Previously, we established that we could selectively decorate cancer cells with antigen-pHLIP conjugates to facilitate antibody recruitment and subsequent killing by engineered effector cells via antibody-dependent cellular cytotoxicity (ADCC). Here, we present a novel strategy for opsonizing antibodies on target cell surfaces using click chemistry. We utilize pHLIP to facilitate selective tetrazine - trans-cyclooctene ligation of human IgGs to the cancer cell surface and induce ADCC. We demonstrate that our approach activates the primary ADCC signaling pathway via CD16a (FcγRIIIa) receptors on effector cells and induces the killing of cancer cell targets by engineered NK cells.
目前许多癌症免疫疗法的作用机制是重新引导免疫系统成分识别癌症生物标志物并引发细胞毒性攻击。缺乏通用的肿瘤生物标志物限制了这些方法的治疗潜力。然而,几乎所有实体瘤的一个特征是细胞外酸性。这种内在的酸性为通过pH低插入肽(pHLIP)进行靶向药物递送提供了基础,pHLIP由于pH依赖性膜插入倾向而在体内肿瘤中选择性积累。此前,我们证实可以用抗原-pHLIP偶联物选择性地修饰癌细胞,以促进抗体募集,并随后通过工程效应细胞通过抗体依赖性细胞毒性(ADCC)进行杀伤。在此,我们提出一种使用点击化学在靶细胞表面调理抗体的新策略。我们利用pHLIP促进人IgG与癌细胞表面的选择性四嗪-反式环辛烯连接,并诱导ADCC。我们证明我们的方法通过效应细胞上的CD16a(FcγRIIIa)受体激活主要的ADCC信号通路,并诱导工程化NK细胞杀伤癌细胞靶标。