The role of BDNF in promoting M2-type macrophage polarization of DRG in glioblastoma with herpes zoster virus infection

Abstract Presently, over 150 therapeutic approaches have been documented for addressing painful gliomas, yet their efficacy remains uncertain due to the lack of a precise understanding of the mechanisms governing glioblastoma herpes zoster virus infection (Hsp) pain.herpes zoster virus infection, commonly known as shingles, is often associated with severe pain. This pain can be quite debilitating and is one of the hallmark symptoms of shingles In this study, we illuminate the dependence of Brain-Derived Neurotrophic Factor (BDNF) on regulatory T cells (Tregs) and delineate how BDNF's interaction with the TRKB signaling pathway contributes to fostering M2 macrophage polarization. Furthermore, we endeavor to elucidate the immune system's role in pain modulation by Hsp infection that regulatory T cells exert an influence on the BDNF/TrkB signaling axis, thereby altering macrophage polarization. We seeks to unravel the intricate connection between solid cellular immunity and Hsp infection glioblastoma, delving into its underlying pathogenesis. By achieving this, our project provided a framework, introducing the concept of employing Treg/BDNF/TrkB/macrophage/DRG interactions as a treatment strategy for Hsp infection glioma-induced pain. The recognition of T cells' involvement in glioma formation and the elucidation of neuropathic pain's pathophysiology through the modulation of macrophage types pave the way for innovative therapeutic interventions. This endeavor promises novel pharmacological targets, therapeutic strategies, and drug development schemes, poised to revolutionize the clinical management of painful gliomas with Hsp infection.