Immunotherapies for cancer aim to induce the immune system to combat cancer cells more effectively. In the journal Angewandte Chemie International Edition, a Chinese research team has now described a new, modular strategy for T-cell-based immunotherapy that manages to work without complex genetic modifications. Modulation of cell–cell communications through an ingenious regulatory circuit using various small, specially folded DNA molecules (aptamers) causes cancer cells to directly activate their mortal enemies, T cells.
Led by Weihong Tan and Liping Qiu, the team developed a regulatory circuit consisting of two modules: 1) recognition-then-triggering and 2) aggregation-then-activation. The circuit is based on different DNA aptamers—short DNA segments that fold into a preprogrammed 3D structure and recognize specific target molecules.
The DNA for module 1 is initially inactive and partially paired into a double strand. If cancer cells are present, the aptamer portion of the recognition single strand binds to protein tyrosinase kinase 7, a protein found in large numbers on the surface of manycells. This splits the DNA double strand, releasing the triggering strand, which triggers module 2.
Module 2 requires two more types of aptamer. Both specifically bind to CD28 immunoreceptors on the surfaces of T cells. CD28 is a co-stimulator in the activation of T cells. This triggering strand binds to an additional loop on a type 1 aptamer. The loop opens and the newly released end binds to a type 2 aptamer, which then binds another type 1 aptamer, and so on .
This results in a double strand and the bound CD28 receptors aggregate, triggering a signal cascade that massively amplifies the activation of T cells. In this way, short-circuited cell communication causesZhimin Wang et al, An Aptamer‐Functionalized DNA Circuit to Establish an Artificial Interaction between T Cells and Cancer Cells,
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