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The homozygous  mutation (p.Cys28Gly) is likely responsible for the inflammation phenotype in this family.  is an ubiquitously expressed serine peptidase that removes tripeptides from the N-terminal end of longer peptides. TPP2 is involved in various biological processes including the destruction of major histocompatibility complex Class I epitopes. Recessive loss-of-function mutations in  were described in patients with Evans syndrome, a rare autoimmune disease affecting the hematopoietic system. Based on the gene expression results in our MS autopsy brain samples, we further suggest that  may play a broader role in the inflammatory process in MS.

TPP2 mutation associated with sterile brain inflammation mimicking MS