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B-cells are abnormal in psychosocial stress and regulate meningeal myeloid cell activation.

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Kigar, Stacey L 
Lehmann, Michael L 
DePuyt, Allison E 
Tuong, Zewen Kelvin 


There is increasing interest in how immune cells, including those within the meninges at the blood-brain interface, influence brain function and mood disorders, but little data on humoral immunity in this context. Here, we show that in mice exposed to psychosocial stress, there is increased splenic B cell activation and secretion of the immunoregulatory cytokine interleukin (IL)-10. Meningeal B cells were prevalent in homeostasis but substantially decreased following stress, whereas Ly6Chi monocytes increased, and meningeal myeloid cells showed augmented expression of activation markers. Single-cell RNA sequencing of meningeal B cells demonstrated the induction of innate immune transcriptional programmes following stress, including genes encoding antimicrobial peptides that are known to alter myeloid cell activation. Cd19-/- mice, that have reduced B cells, showed baseline meningeal myeloid cell activation and decreased exploratory behaviour. Together, these data suggest that B cells may influence behaviour by regulating meningeal myeloid cell activation.



B cells, Behaviour, Immunity, Meninges, Myeloid, Stress, Animals, Antigen Presentation, B-Lymphocytes, Meninges, Mice, Mice, Inbred C57BL, Myeloid Cells, Stress, Psychological

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Brain Behav Immun

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Elsevier BV
Medical Research Council (MR/N024907/1)
Arthritis Research UK (21777)
MRC (MR/S006257/1)
Cambridge University Hospitals NHS Foundation Trust (CUH) (BRC)
Department of Health (via National Institute for Health Research (NIHR)) (156239)
Medical Research Council (MC_G0802534)
Medical Research Council (MR/L014815/1)
M.R.C. is supported by a Medical Research Council New Investigator Research Grant (MR/N024907/1); Versus Arthritis Cure Challenge Research Grant (21777); and National Institute for Health Research (NIHR) Research Professorship (RP-2017-08-ST2-002). M.E.L. is supported by a fellowship and grant from Addenbrooke’s Charitable Trust, Cambridge and a fellowship from the Medical Research Council (MR/S006257/1). E.T.B is supported by an NIHR Senior Investigator award. M.R.C., E.T.B., and M.E.L. are also supported by the Cambridge NIHR Cambridge Biomedical Research Centre (BRC). A.E.D., M.L.L., S.L.K., S.J.L., and M.H. are supported by NIH Intramural Research Program NIMH ZIA MH001090. A.G.E. is supported by NIH Intramural Research Program NHGRI HG200365-09.