bims-hypusi Biomed News
on Hypusine and eIF5A
Issue of 2025–03–23
two papers selected by
Sebastian J. Hofer, University of Graz



  1. Immunotargets Ther. 2025 ;14 205-226
       Background: The generation of functionally active, stable T regulatory cells (Tregs) is a crucial target of type 1 diabetes (T1D) immunotherapy. This study investigated therapeutic intervention for T1D/Latent autoimmune diabetes in adults (LADA), wherein the diabetogenic proinflammatory Treg (intermediate) cell subset was characterized and driven to a Treg phenotype (CD4+CD25+FOXP3+). This involved simultaneous inhibition of the eukaryotic initiation factor 5a (eIF5a) and Notch pathways using GC7 (N1-Guanyl-1,7-diaminoheptane) and Anti-DLL4 (Delta-like-ligand-4).
    Methods: Peripheral blood from patients with T1D/LADA and healthy adults (n=7 each) was used to isolate the CD4+CD25- T cell population and CD4 deficient peripheral blood mononuclear cells (PBMCs). Cells were subjected to GAD65+GC7+anti-DLL4 treatment for seven days and compared with conventional anti-CD3/CD28/CD137 stimulation for conversion into the Tregs. Newly plasticized Tregs were assessed for their suppressive potential against freshly isolated autologous T responder cells. In addition, live, dead, and apoptotic cell counts were performed to evaluate the adverse effects of immunomodulatory treatment on immune cells. The data was analyzed with GraphPad Prism using 1- or 2-way ANOVA and a Student's t-test.
    Results: A unique population of proinflammatory cytokines expressing intermediate Tregs (CD4+CD25-IFNg+IL17+FOXP3+) was characterized in T1D/LADA patients and found significantly increased compared to age-matched healthy adults. Simultaneous inhibition of eIF5a and Notch pathways could induce Treg phenotype in Treg-deficient CD4+ T cells and CD4 deficient PBMCs from T1D/LADA patients. GAD65+GC7+anti-DLL4 treatment plasticized Tregs withstanding a proinflammatory milieu mimicking T1D/LADA, and the plasticized Tregs exhibited a stable and suppressive functional phenotype. Furthermore, GAD65+GC7+anti-DLL4 treatment had no adverse effects on immune cells.The present approach is a multipronged approach involving the inhibition of eIF5a and Notch pathways that addresses the upregulation of immune tolerance, differentiation, and proliferation of cytotoxic T cells and alleviates β-cell dysfunction. Additionally, this treatment strategy could also be leveraged to boost Treg generation following islet transplantation or as a combinational therapy along with adoptive cell transfer.
    Keywords:  autoimmune disorders; eIF5a; immune cell plasticity; immunomodulation; latent autoimmune diabetes in adults; notch; transdifferentiation; type 1 diabetes; unfit tregs
    DOI:  https://doi.org/10.2147/ITT.S504555
  2. PLoS One. 2025 ;20(3): e0319280
      Protein synthesis involves translation initiation, elongation, termination, and ribosome recycling, and each step is controlled intricately by many signaling proteins. Translation initiation can be compactly categorized into two mechanisms: primary and secondary. The primary mechanism involves the recruitment of three important eukaryotic initiation factors, eIF2-GDP, eIF5, and eIF2B, and their interactions, followed by the GDP-GTP exchange by eIF2B to form an active dimer eIF2-GTP. The dimer binds with Met-tRNA to form a robust ternary complex (TC). The secondary mechanism closely mirrors the primary reaction mechanism, except that the interactions of eIF2B and eIF5 happen with the TC to form complexes. These interactions happen with high fidelity and precision, failing which fail-safe mechanisms are invoked instantaneously to delay the initiation process. In this work, we build a mathematical model to unravel how the transition between translation initiation and termination occurs at the initiation stage based on the elementary mechanisms we built from the network assembled from experimental observations. We focus only on the dynamics of primary and secondary mechanisms involved in the translation initiation process under normal and integrated stress response (ISR) conditions that act as a fail-safe mechanism by through phosphorylation-dephosphorylation (PdP) reactions. Since the network is huge and has many unknown kinetic parameters, we perform structural analysis using chemical reaction network theory (CRNT) and find hidden positive feedback loops that regulate the initiation mechanism. We apply bifurcation theory to show that the model exhibits ultrasensitivity and bistability under normal conditions, while under ISR, it exhibits both bistability and tristability for the choice of kinetic parameters. We attribute bistability to translation initiation and termination and tristability in ISR to translation recovery and attenuation. We conclude that the translation initiation process is a highly regulated process guided by the threshold and switching mechanisms to make quick decisions on the translation initiation, termination, recovery or attenuation under different conditions.
    DOI:  https://doi.org/10.1371/journal.pone.0319280