Heterogeneous Nuclear Ribonucleoprotein K Autoantibodies in Patients who Suffered Severe Traumatic Brain Injury

The immune-inflammatory response as well as cerebral endothelial activation has been described after Traumatic Brain Injury (TBI). Although inflammation can have both beneficial and detrimental effects in TBI, the mechanisms underlying this dichotomy are mostly unknown. Moreover, emerging data indicates that chronic alterations produced after TBI are probably the result of systemic and persistent inflammation that activates immune response, culminating in the production of different specific auto antibodies against central nervous system antigens. In the previous study we demonstrated the production of anti-hnRNPK antibodies, belonging to Anti-Endothelial Cell Antibodies (AECA), in heart transplanted patients who developed Cardiac Allograft Vasculopathy (CAV). These antibodies could be produced in response to the vascular endothelial damage that is also present in TBI patients. In the current study we analyse the presence of AECA by Indirect Immunofluorescence assay (IFI) and anti-hnRNPK IgG antibodies by Enzyme-Linked Immunosorbent Assay (ELISA) in a cohort of 19 patients who suffered TBI. We detected a significant increase in the number of patients with AECA and anti-hnRNPK antibodies after TBI. Moreover, anti-hnRNPK antibody levels were also higher during follow-up, being the values obtained after TBI significantly higher than those detected at the time of trauma (p = 0.001). We also found that AECA and anti-hnRNPK antibodies were mostly present in the sera of patients with a worse outcome (p = 0.018 and p = 0.04 respectively). Taking into account, measuring these auto antibodies could be useful for evaluating endothelial injury and/or the outcome after TBI.