2026/03/01 by Sheng Yang, Hang Zhang, Lulu Xu +13 · 1 voice
Immunology and Microbiology · Neuroscience · #Macrophage Migration Inhibitory Factor #Neuroinflammation and Neurodegeneration Mechanisms #Nuclear Receptors and Signaling
paper · doi:10.1172/jci196905
openalex created_date 2026/03/01 · openalex publication_date 2026/03/01 · openalex updated_date 2026/07/28
Neuroinflammation, encompassing both innate and adaptive immune responses, plays a crucial role in ischemic stroke. Although B lymphocytes are central to adaptive immunity, their contributions to ischemic stroke remain poorly understood. Here, we demonstrated that B lymphocytes accumulate in ischemic lesions, forming germinal center-like structures at the later stage after stroke, which mainly depended on in situ proliferation. This accumulation correlated with worsened neuroinflammation and ischemic injury, whereas B cell depletion reduced chronic brain damage during stroke. Mechanistically, microglia recruited B cells into ischemic lesions through MIF-CD74/CXCR4 signaling during the early phase of stroke, while IFN-related pathways in B cells further drove neuroinflammation and brain injury. Targeting these pathways markedly alleviated cerebral ischemia and inflammation. Our findings shed light on the role of B lymphocytes in stroke pathology and suggest promising new avenues for therapeutic intervention.