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Complement membrane attack complex and protectin (CD59) in liver allografts during acute rejection.
I Lautenschlager1, K Höckerstedt, S Meri
1Fourth Department of Surgery, Helsinki University Central Hospital and University of Helsinki, Finland.
Journal of Hepatology
|September 17, 1999
Summary
Complement activation and membrane attack complex (MAC) deposition occur during liver allograft rejection. A decrease in CD59 expression on neutrophils may increase susceptibility to complement-mediated damage.
Area of Science:
- Immunology
- Transplantation immunology
Background:
- The complement system plays a role in xenograft rejection, but its role in allograft rejection is less understood.
- Membrane attack complex (MAC) mediates complement lysis and is inhibited by CD59 (protectin).
Purpose of the Study:
- To investigate MAC deposition and CD59 expression in liver allograft rejection.
- To correlate these findings with immune activation markers.
Main Methods:
- Liver allografts were monitored using fine-needle aspiration biopsies (FNAB).
- Immunoperoxidase staining was employed to detect MAC, CD59, and rejection markers (IL2-receptor, MHC class II, ICAM-1).
Main Results:
- Acute rejection episodes showed increased expression of IL2-receptor, MHC class II, and ICAM-1.
- MAC deposition was observed in infiltrating leukocytes and parenchymal cells during rejection.
- CD59 expression decreased significantly in neutrophils but varied in other cells.
Conclusions:
- Complement activation and MAC assembly are associated with acute liver allograft rejection.
- Reduced CD59 expression may contribute to complement-mediated cell elimination during rejection.