Immune response and histology of humoral rejection in kidney transplantation.
The adaptive immune response forms the basis of allograft rejection. Its weapons are direct cellular cytotoxicity, identified from the beginning of organ transplantation, and/or antibodies, limited to hyperacute rejection by preformed antibodies and not as an allogenic response. This resulted in allogenic response being thought for decades to have just a cellular origin. But the experimental studies by Gorer demonstrating tissue damage in allografts due to antibodies secreted by B lymphocytes activated against polymorphic molecules were disregarded. The special coexistence of binding and unbinding between antibodies and antigens of the endothelial cell membranes has been the cause of the delay in demonstrating the humoral allogenic response. The endothelium, the target tissue of antibodies, has a high turnover, and antigen-antibody binding is non-covalent. If endothelial cells are attacked by the humoral response, immunoglobulins are rapidly removed from their surface by shedding and/or internalization, as well as degrading the components of the complement system by the action of MCP, DAF and CD59. Thus, the presence of complement proteins in the membrane of endothelial cells is transient. In fact, the acute form of antibody-mediated rejection was not demonstrated until C4d complement fragment deposition was identified, which is the only component that binds covalently to endothelial cells. This review examines the relationship between humoral immune response and the types of acute and chronic histological lesion shown on biopsy of the transplanted organ.
Nephrology Department, Regional University Hospital of Malaga, Malaga University, IBIMA, REDINREN RD12/0021/0015, Malaga, Spain. Electronic address: mgonmol@yahoo.es.
Miguel
M
González-Molina
Nephrology Department, Regional University Hospital of Malaga, Malaga University, IBIMA, REDINREN RD12/0021/0015, Malaga, Spain.
Pedro
P
Ruiz-Esteban
Immunology Department, Regional University Hospital of Malaga, Malaga University, IBIMA, REDINREN RD12/0021/0015, Malaga, Spain.
Abelardo
A
Caballero
Nephrology Department, Regional University Hospital of Malaga, Malaga University, IBIMA, REDINREN RD12/0021/0015, Malaga, Spain.
Dolores
D
Burgos
Nephrology Department, Regional University Hospital of Malaga, Malaga University, IBIMA, REDINREN RD12/0021/0015, Malaga, Spain.
Mercedes
M
Cabello
Pathology Department, Regional University Hospital of Malaga, Malaga University, IBIMA, REDINREN RD12/0021/0015, Malaga, Spain.
Miriam
M
Leon
Nephrology Department, Regional University Hospital of Malaga, Malaga University, IBIMA, REDINREN RD12/0021/0015, Malaga, Spain.
Laura
L
Fuentes
Nephrology Department, Regional University Hospital of Malaga, Malaga University, IBIMA, REDINREN RD12/0021/0015, Malaga, Spain.
Domingo
D
Hernandez
D000818:Animals; D001706:Biopsy; D015935:Complement C4b / Q000276:immunology; D003171:Complement Pathway, Classical; D042783:Endothelial Cells / Q000276:immunology; D006084:Graft Rejection / Q000175:diagnosis / Q000276:immunology*; D006183:H-2 Antigens / Q000276:immunology; D006680:HLA Antigens / Q000276:immunology; D006801:Humans; D056724:Immunity, Humoral / Q000276:immunology*; D007518:Isoantibodies / Q000276:immunology; D007668:Kidney / Q000098:blood supply / Q000276:immunology / Q000473:pathology; D016030:Kidney Transplantation; D008214:Lymphocytes / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D018448:Models, Immunological; D009504:Neutrophils / Q000276:immunology; D010446:Peptide Fragments / Q000276:immunology; D014181:Transplantation Immunology
D006183:H-2 Antigens; D006680:HLA Antigens; D007518:Isoantibodies; D010446:Peptide Fragments; D015935:Complement C4b; C032261:complement C4d
Antibodies; Anticuerpos; Biopsia renal; Humoral rejection; Immune response; Rechazo humoral; Renal biopsy; Respuesta inmune