Tranexamic acid modulates the cellular immune profile after traumatic brain injury in mice without hyperfibrinolysis.
Dominik F DraxlerMaria DaglasAnushka FernandoGryselda HanafiFiona McCutcheonHeidi HoAdam GalleJulia GregoryPia LarssonCharithani KeragalaDavid K WrightElnaz TavanchehAmanda E AuBe'eri NiegoKirsty WilsonMagdalena PlebanskiMaithili SashindranathRobert L MedcalfPublished in: Journal of thrombosis and haemostasis : JTH (2019)
In the absence of systemic hyperfibrinolysis, plasmin deficiency or blockade with TXA increases migration and proliferation of conventional dendritic cells (cDCs) and various antigen-presenting cells and T cells in the draining cervical lymph node (cLN) post TBI. Tranexamic acid might also be clinically beneficial in modulating the inflammatory and immune response after TBI, but without promoting CNS autoreactivity.
Keyphrases
- dendritic cells
- immune response
- lymph node
- traumatic brain injury
- induced apoptosis
- signaling pathway
- severe traumatic brain injury
- cell cycle arrest
- mild traumatic brain injury
- regulatory t cells
- oxidative stress
- blood brain barrier
- neoadjuvant chemotherapy
- high fat diet induced
- toll like receptor
- case report
- sentinel lymph node
- endoplasmic reticulum stress
- type diabetes
- adipose tissue
- early stage
- insulin resistance