Spinal cord injury impacts B cell production, homeostasis, and activation

• Bone marrow B lymphopoiesis transiently ceases after SCI injury but resumes within 4 weeks post SCI.
• Peripheral B cell subsets are differentially affected by SCI; follicular and transitional B cell numbers are acutely reduced, whereas marginal zone B cells are preserved.
• Follicular B cell numbers are chronically depressed, possibly reflecting a sustained reduction in systemic BLyS.
• T cell dependent humoral immune responses are normal after SCI, but T independent responses are blunted.
• Preexisting humoral immunologic memory is retained following SCI.

Complex interactions govern the interplay of central nervous and immune systems, including the generation, homeostatic maintenance, and activation of B cells. Accordingly, spinal cord injury will likely impact all of these processes. Several laboratories have recently explored this possibility, and their observations in aggregate reveal both acute and chronic consequences that can vary based on the injury location. Acute effects include a transient cessation of bone marrow B lymphopoiesis, with a corresponding drop in the peripheral follicular and transitional B cell subsets, whereas the marginal zone subset is preserved. Despite recovery of B lymphopoiesis by 28 days post injury, follicular B cell numbers remain depressed; this may reflect reduced levels of the homeostatic cytokine BLyS. In general, the ability to mount T dependent antibody responses after injury are intact, as are pre-existing memory B cell pools and antibody levels. In contrast, T-independent responses are chronically compromised. Both glucocorticoid-dependent and -independent processes mediate these effects, but a detailed understanding of the mechanisms involved awaits further study. Nonetheless, these observations in toto strengthen the growing appreciation for bidirectional interactions between the CNS and immune system, highlighting the need for further basic and translational efforts.