Trends Immunol. 2025 Oct 22:S1471-4906(25)00244-3. doi: 10.1016/j.it.2025.09.009. Online ahead of print.

ABSTRACT

Traumatic brain injury (TBI) is a leading cause of neurological disability, associated with higher rates of cognitive complications that negatively affect recovery. Myriad cytokine and chemokine pathways propagate the secondary responses to injury. This review discusses the integration of peripheral and central immune cytokine and chemokine signaling cascades after TBI and recovery, with a focus on preclinical work. We first discuss key cytokine and chemokine interactions influencing recovery and long-term deficits. Next, we discuss the major cell types that propagate and respond to the inflammatory process after TBI. Understanding neuroimmune signaling, utilizing recent advances in transcriptomics and immune profiling, with a focus on cytokines and chemokine after TBI reveals therapeutic targets and informs strategies to improve long-term recovery and outcomes.

PMID:41130893 | DOI:10.1016/j.it.2025.09.009