B cell treatment promotes a neuroprotective microenvironment after traumatic brain injury through reciprocal immunomodulation with infiltrating peripheral myeloid cells.

The CD45 mid CNS-resident microglia also showed an overall trend towards a less inflammatory functional phenotype in animals treated with B cells at the time of injury.

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We used intravenous administration of clodronate liposomes to specifically deplete highly phagocytic CD45 hi CD11b hi monocytes/macrophages, and confirmed that the systemic depletion translated into a highly significant reduction of approximately 90% in the number of monocytes/macrophages infiltrating the brain at 48 h after CCI (Fig. 7 B, C).

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