Cell memory

Cell memory is the ability of a cell to retain information about previous exposures, conditions, or functional states and use that information to shape its future behavior.

Traditionally, cellular memory has been explained mainly through genetic and epigenetic mechanisms. Our work expands this concept by showing that cell memory is governed through the Universal Receptive System, including extracellular DNA- and RNA-based regulatory structures known as Teazeled receptors, or TezRs, as well as integrases and recombinases.

This means that a cell’s behavior is not determined only by its genome. It is also influenced by its history. Previous stress, infection, immune activation, drug exposure, or environmental signals can leave a functional “memory” that changes how the cell responds later.

In microorganisms, cell memory helps explain why bacteria exposed to hostile environments later show altered biofilm formation, antibiotic tolerance, resistance patterns, and survival strategies. This is one reason infections in patients often behave differently from organisms tested under simplified laboratory conditions.

The preservation of cell memory is central to the AtbFinder test system. AtbFinder is designed to select antibiotics effective against resistant microorganisms by preserving the functional memory of the microbial community directly from clinical samples. By maintaining this memory, the test is intended to model a more accurate antibiotic response that better reflects what occurs in the patient.

In human immune cells, cell memory is especially important because it affects how leukocytes recognize threats, respond to infection, and attack abnormal cells. By modulating the Universal Receptive System, it becomes possible to change the functional memory of immune cells and shift them into a more active therapeutic state.

This principle forms part of the foundation for the SL-28 cell therapy platform. Through ex vivo modulation, immune cells can be reprogrammed without genetic engineering, allowing them to acquire enhanced antimicrobial and anticancer activity before being returned to the patient.

In this context, cell memory is not just a passive record of the past. It is an active biological mechanism that influences cell identity, adaptation, therapeutic response, and disease progression. Understanding and controlling cell memory opens a new path for developing therapies in oncology, infectious disease, aging, and immune-mediated conditions.

References
  1. Tetz V, Tetz G. “Novel prokaryotic system employing previously unknown nucleic acids-based receptors.” Microbial Cell Factories. 2022;21:1–33. DOI: 10.1186/s12934-022-01923-0.
  2. Tetz V, Tetz G. “Novel Cell Receptor System of Eukaryotes Formed by Previously Unknown Nucleic Acid-Based Receptors.” DNA. 2022.
  3. Tetz G, Kardava K, Vecherkovskaya M, Khodadadi-Jamayran A, Tsirigos A, Tetz V. “Universal receptive system as a novel regulator of transcriptomic activity of Staphylococcus aureus.” Microbial Cell Factories. 2025;24:1. DOI: 10.1186/s12934-024-02637-1.
  4. Tetz V, Kardava K, Vecherkovskaya M, Khodadadi-Jamayran A, Tsirigos A, Tetz G. “Previously unknown regulatory role of extracellular RNA on bacterial directional migration.” bioRxiv / PubMed preprint record. 2024.
  5. Tetz V, Kardava K, Vecherkovskaya M, Khodadadi-Jamayran A, Tsirigos A, Tetz G. “Regulating white blood cell activity through the novel universal receptive system.” Scientific Reports. 2025.
  6. Tetz V, Kardava K, Vecherkovskaya M, Khodadadi-Jamayran A, Tsirigos A, Tetz G. “The Universal Receptive System acts as a novel regulator in the production of antimicrobial and anticancer bioactive compounds by white blood cells.” Journal of Leukocyte Biology. 2025.
  7. Tetz V, Kardava K, Vecherkovskaya M, Khodadadi-Jamayran A, Tsirigos A, Tetz G. “Dramatic Clinical Response to a Novel Form of Cell Therapy SL-28 in a Patient With Advanced Prostate Cancer: A Case Report.” ImmunoTargets and Therapy. 2025.
  8. “Partial response in a patient with skeletal and hepatic metastases following resected pancreatic cancer to the novel cell therapy SL-28: a case report.” Frontiers in Oncology. 2025.