Background Natural killer (NK) cells comprise the main components of
lymphocyte-mediated nonspecific immunity. Through their effector function they
play a crucial role combating bacterial and viral challenges. They are also
thought to be key contributors to the systemic spinal cord injury-induced
immune-deficiency syndrome (SCI-IDS). SCI-IDS increases susceptibility to
infection and extends to the post-acute and chronic phases after SCI. Methods
and design The prospective study of NK cell function after traumatic SCI was
carried out in two centers in Berlin, Germany. SCI patients and control
patients with neurologically silent vertebral fracture also undergoing
surgical stabilization were enrolled. Furthermore healthy controls were
included to provide reference data. The NK cell function was assessed at 7
(5–9) days, 14 days (11–28) days, and 10 (8–12) weeks post-trauma. Clinical
documentation included the American Spinal Injury Association (ASIA)
impairment scale (AIS), neurological level of injury, infection status,
concomitant injury, and medications. The primary endpoint of the study is
CD107a expression by NK cells (cytotoxicity marker) 8–12 weeks following SCI.
Secondary endpoints are the NK cell’s TNF-α and IFN-γ production by the NK
cells 8–12 weeks following SCI. Discussion The protocol of this study was
developed to investigate the hypotheses whether i) SCI impairs NK cell
function throughout the post-acute and sub-acute phases after SCI and ii) the
degree of impairment relates to lesion height and severity. A deeper
understanding of the SCI-IDS is crucial to enable strategies for prevention of
infections, which are associated with poor neurological outcome and elevated
mortality. Trial registration DRKS00009855