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. Author manuscript; available in PMC: 2025 Jan 1.
Published in final edited form as: Trends Mol Med. 2023 Nov 7;30(1):10–12. doi: 10.1016/j.molmed.2023.10.007

Figure 1. Systemic PF4 treatment in aged mice mitigates peripheral and hippocampal inflammation to improve cognitive function.

Figure 1.

Systemic treatment of aged mice with PF4 results in changes in innate and adaptive immune function in the periphery, including reduced levels of myeloid/neutrophil inflammatory signals and reduced age-related exhaustion and cytotoxic T cell markers with concomitant improvements in hippocampus-dependent learning and memory, synapse function, and microglial activation. Mice lacking CXCR3 exhibit a partial loss of PF4-mediated CNS benefits, raising the possibility that CXCR3-expressing T cells are critical for the effects of PF4. Changes in the CNS following PF4 treatment may be mediated by shifts in peripheral cytokines, immune cell infiltration, or direct action of PF4, though future studies will clarify the relative contributions of these mechanisms and PF4’s regulation of neuroimmune interactions in the CNS. Abbreviations: CXCR3, C-X-C Motif Chemokine Receptor 3; CNS, central nervous system; PF4, platelet factor 4. This figure was created with tools from BioRender.com.