Here, a role for T-lymphocytes in secondary axonal injury was demonstrated.by crossbreeding V(D)J recombination activation (Rag1) knockout mice, which lack mature T and B lymphocytes, to a model of the leukodystrophy PMD, caused by overexpression of the proteolipid PLP1 gene (see Mechanisms of injury: axonal pathology downstream of oligodendroglial defects), in which axonal changes were reduced when lymphocytes were depleted. Here, PLP1 is linked to Pelizeaus-Merzbacher spectrum disorder.