Igor Smirnov

TL;DR: It is demonstrated in an experimental mouse model of TBI that mild forms of brain trauma cause severe deficits in meningeal lymphatic drainage that begin within hours and last out to at least one month post-injury.

TL;DR: This paper showed that ablation of meningeal lymphatic vessels in 5xFAD mice (a mouse model of amyloid deposition that expresses five mutations found in familial AD) worsened the outcome of mice treated with anti-Aβ passive immunotherapy by exacerbating the deposition of Aβ, microgliosis, neurovascular dysfunction, and behavioural deficits.

TL;DR: Transfer of a monoclonal T cell population reactive to the central nervous system (CNS) antigen, myelin oligodendrocyte glycoprotein (MOG), was sufficient to improve cognitive task performance in otherwise impaired OTII mice, raising the possibility that the antigen-specificity requirement of pro-cognitive T cells may be directed against CNS-derived self-antigens.

TL;DR: Results suggest that the DC-mediated neuroprotection was achieved via the induction of a systemic T-cell-dependent immune response, and the use of antigen-specific DCs may represent an effective way to obtain the maximal benefit of immune-mediated repair and maintenance as well as protection against self-destructive compounds.

TL;DR: Type 2 innate lymphocytes (ILC2s) are described as a novel cell type resident in the healthy meninges that are activated after CNS injury and could lead to new therapeutic insights for neuroinflammatory conditions.