Neuroinflammation　after　traumatic　brain　injury　(TBI)　is　related　to　chronic　neurodegenerative　diseases　and　is　one　of　the　causes　of　acute　secondary　injury　after　TBI.　Therefore,　it　is　particularly　important　to　clarify　the　role　of　cellular　mechanisms　in　the　neuroinflammatory　response　after　TBI.　The　objective　of　this　article　is　to　understand　the　involvement　of　cells　during　the　TBI　inflammatory　response　(for　instance,　astrocytes,　microglia,　and　oligodendrocytes)　and　shed　light　on　the　recent　progress　in　the　stimulation　and　interaction　of　granulocytes　and　lymphocytes,　to　provide　a　novel　approach　for　clinical　research.　We　searched　articles　in　PubMed　published　between　1950　and　2023,　using　the　following　keywords:　TBI,　neuroinflammation,　inflammatory　cells,　neuroprotection,　clinical.　Articles　for　inclusion　in　this　paper　were　finalized　based　on　their　novelty,　representativeness,　and　relevance　to　the　main　arguments　of　this　review.　We　found　that　the　neuroinflammatory　response　after　TBI　includes　the　activation　of　glial　cells,　the　release　of　inflammatory　mediators　in　the　brain,　and　the　recruitment　of　peripheral　immune　cells.　These　inflammatory　responses　not　only　induce　secondary　brain　damage,　but　also　have　a　role　in　repairing　the　nervous　system　to　some　extent.　However,　not　all　of　the　mechanisms　of　cell-to-cell　interactions　have　been　well　studied.　After　TBI,　clinical　treatment　cannot　simply　suppress　the　inflammatory　response,　and　the　inflammatory　phenotype　of　patients＇　needs　to　be　defined　according　to　their　specific　conditions　after　injury.　Clinical　trials　of　personalized　inflammation　regulation　therapy　for　specific　patients　should　be　carried　out　in　order　to　improve　the　prognosis　of　patients.