| 초록 |
Anti-HLA donor-specific antibodies (DSA) induce both acute and chronic antibody-mediated rejection, and thereby
contribute to graft loss. Interestingly, high panel reactive antibody status influenced graft outcomes even in HLAidentical
siblings, who do not have DSA. Recently, many anti-non-HLA antibodies have been detected and reported to
have prognostic values.
Both danger and alloimmunity can induce tissue injury, and autoimmunity to cryptic self antigens such as collagen,
K-α1 tubulin, LG-3, vimentin, myosin etc. Antibodies against angiotensin type 1 receptor (AT1R), endothelin type A
receptor, and major histocompatibility complex class I-related chain A (MICA) are also produced. Anti-non-HLA
antibodies can induce inflammation by complement or antibody-dependent cellular cytotoxicity, coagulation by tissue
factor, and fibrosis by growth factors.
Anti-MICA does not seem to have significant impact on renal allograft survival in modern immunosuppression. Both
pre-transplant and de novo post-transplant anti-AT1R antibodies have significant impact on renal allograft survival
independently of DSA. Anti-LG3 antibodies were associated with obliterative renal allograft vasculopathy. Anti-apoptotic
cell antibodies were also associated with allograft outcomes independently of DSA. However, current guidelines do not
recommend solid phase assays or endothelial cell cross-match for anti-non-HLA antibodies as a routine exam, because
their prognostic values remain uncertain and high cost.
Combination anti-humoral therapy including plasmapheresis, intravenous immunoglobulin, rituximab, and bortezomib
is expected to inhibit anti-non-HLA antibody-mediated injury. AT1R antagonist has also a role in anti-AT1R antibodymediated
injury. |