Our data suggest that application of non-competitive NMDARantagonists during chronic treatments of neurological disorders like Alzheimer`sdisease may not only involve neuronal NMDARs, but may also have additiveside-effects by targeting B cells, which are assumed to contribute to thesedisorders [7,9,10].Given that the drugs impaired several B-cell functions, but enhanced IL-10production in BCR/CD40-stimulated B cells, their employment in systemic inflammationor autoimmune diseases, for instance in sepsis or anti-NMDAR encephalitis, appearspromising. This evidence concerns the gene CD40 and autoimmune disease.