Antibodies have always been the biggest concern in transplantation. During vascular rejection, there is endothelial cell damage. The apoptotic endothelial cells release a fragment of perlecan referred as LG3.
A recent study in the AJT identified a novel antibody that may be playing a role in vascular form of antibody mediated rejection. The authors call this anti-LG3, an antibody that some patients produce to attack a protein that plays an important role in vascular repair and regeneration, LG3. In these patients, the secretion of LG3 by the new kidney stimulates the activity of these antibodies which attack and injure the blood vessels of the transplanted organ, and the normal healing process of the transplanted organ is impaired. Patients who experienced vascular rejection had elevated anti-LG3 titers pre and posttransplantation compared to subjects with interstitial form of rejection( cellular) or stable graft function significantly respectively. The authors also confirmed these findings with mice data. Collectively, these data identify anti-LG3 antibodies as novel accelerators of immune-mediated vascular injury and obliterative remodeling. One prior animal study showed similar findings.
Do we have a new marker for potential vascular rejection? What is the data on LG3 in other forms of endothelial injury namely CNI induced TMA or other forms of endothelial damage? Then again, the perlecans are altered in certain genetic diseases that don't quite fit the role they play in transplantation.