TMEM176A and TMEM176B Are Candidate Regulators of Inhibition of Dendritic Cell Maturation and Function after Chronic Spinal Cord Injury.

Inhibition of dendritic cell maturation and activation, together with abnormal functioning of cell-mediated immunity, has been reported in chronic spinal cord injury (SCI). The development of immune-based therapies could: 1) prevent or slow down limit further tissue damage in chronic SCI, and 2) promote tissue regeneration. To identify novel candidate molecular pathways mediating SCI-induced immune changes, we performed whole-genome microarray and molecular pathway analyses.

Neurotoxic or Neuroprotective? Current Controversies in SCI-Induced Autoimmunity.

Controversy exists regarding the autoimmune response that has been observed following traumatic spinal cord injury (SCI). It is not clear if this represents a protective response by the immune system to prevent further tissue damage, a pathological reaction of the immune system to central nervous system antigens released by the injury, or a combination of both. Experimental evidence indicates that B cells produce auto-antibodies following SCI and that the presence of self-reactive antibodies is associated with tissue damage.

B-cell maturation antigen, a proliferation-inducing ligand, and B-cell activating factor are candidate mediators of spinal cord injury-induced autoimmunity.

Autoimmunity is thought to contribute to poor neurological outcomes after spinal cord injury (SCI). There are few mechanism-based therapies, however, designed to reduce tissue damage and neurotoxicity after SCI because the molecular and cellular bases for SCI-induced autoimmunity are not completely understood. Recent groundbreaking studies in rodents indicate that B cells are responsible for SCI-induced autoimmunity.