Unravelling the role of the immune receptor CD300f in spinal cord injury and metabolic reprogramming

Project Details


Inflammation after spinal cord injury (SCI) exerts a key effect on the progress of both degeneration and regeneration after a
traumatic injury. In addition, it has become increasingly clear that understanding the interaction between metabolism and
immune function can provide an insight into cellular responses to different challenges. Recent reports from our group and
others, suggest that metabolic reprogramming and immune receptors play an orchestrated role in modulating microglia and
macrophage phenotype. An interesting example is CD300f, a very unique immune receptor that: i) displays a dual activating/
inhibitory capacity; ii) is important for the phagocytosis of apoptotic cells and putatively of synapses; and iii) regulates
microglia immunometabolic phenotype.
Our hypothesis postulates that, by modulating immunometabolism, CD300f plays an important role in neuroprotection under
neuroinflammatory conditions. In the current project, we propose to addresses the interplay between inflammation and
metabolic reprogramming by evaluating the role of microglia/macrophage CD300f and their metabolic reprogramming after
SCI. We will also test the efficacy of a mitochondrial modulator as a novel neuroprotective strategy for the stimulation of
microglial mitochondrial oxidative metabolism.
This proposal is based on a set of unpublished data produced by both the ER at the Institut Pasteur Montevideo and the host
institution. We will use novel tools generated by our group as the CD300floxP mice, that crossed with CX3CR1-Creert mice
will enable to the conditional CD300f KO in microglia and barrier macrophages, and compare these results with global KO
mice. The results generated will provide novel insights related to the mechanisms underlying SCI, and for the understanding
of how the immune system and the metabolism dialogue in SCI. This could have important implications in a broad spectrum
of neurological diseases, where inflammation contribute detrimentally to the pathology.
Effective start/end date1/10/2130/09/23


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