Chronic spinal cord injury impairs primary antibody responses but spares existing humoral immunity in mice

MA Oropallo, KS Held, R Goenka… - The Journal of …, 2012 - journals.aai.org
MA Oropallo, KS Held, R Goenka, SA Ahmad, PJ O'Neill, O Steward, TE Lane, MP Cancro
The Journal of Immunology, 2012journals.aai.org
Spinal cord injury (SCI) results in immune depression. To better understand how injury
inhibits humoral immunity, the effects of chronic thoracic SCI on B cell development and
immune responses to thymus-independent type 2 and thymus-dependent Ags were
determined. Mice received complete crush injury or control laminectomy at either thoracic
level 3, which disrupts descending autonomic control of the spleen, or at thoracic level 9,
which conserves most splenic sympathetic activity. Although mature B cell numbers were …
Abstract
Spinal cord injury (SCI) results in immune depression. To better understand how injury inhibits humoral immunity, the effects of chronic thoracic SCI on B cell development and immune responses to thymus-independent type 2 and thymus-dependent Ags were determined. Mice received complete crush injury or control laminectomy at either thoracic level 3, which disrupts descending autonomic control of the spleen, or at thoracic level 9, which conserves most splenic sympathetic activity. Although mature B cell numbers were only mildly reduced, bone marrow B cell production was transiently but profoundly depressed immediately after injury. Despite the return of normal B cell production 4 wk after SCI, mice receiving thoracic level 3 injury showed a significant reduction in their ability to mount primary thymus-independent type 2 or thymus-dependent immune responses. The latter were marked by decreases in germinal center B cells as well as class-switched high-affinity Ab-secreting cells. Importantly, injury did not affect affinity maturation per se, pre-existing B cell memory, or secondary humoral immune responses. Taken together, these findings show that chronic high thoracic SCI impairs the ability to mount optimal Ab responses to new antigenic challenges, but spares previously established humoral immunity.
journals.aai.org