IMMUNOSUPPRESSION

IMMUNOSUPPRESSION

Modern immunosuppression is so e ff ective that acute rejec - tion rates of 10–20% can be achieved in all types of solid organ transplantation. The challenge is to deliver su ffi cient immunosuppression to prevent rejection while minimising drug side e ff ects. Imm unosuppression also increases the risk of both infection and malignancy . This is a non-specific e ff ect related to the total burden of immunosuppression rather than agent-specific side e ff ects. The mechanisms of action of current immunosuppressive drugs depend on anti-inflammatory e ff ects and the prevention of lymphocyte activation and proliferation ( Figure 88.10 ). Lymphocytes are some of the most rapidly dividing cells in y and their activation and clonal expansion forms the the bod immunological basis of acute allograft rejection. Immunosuppression for transplantation has two phases: induction and maintenance. Induction therapy commonly consists of a combination of high-dose intravenous steroids and the anti-CD25 monoclonal antibody basiliximab, which locks IL-2 receptors. Other induction agents for high-risk b cases are ATG and the monoclonal antibody alemtuzumab (Campath). The commonest maintenance immunosuppressive regi - men for solid organ transplants consists of triple therapy with a calcineurin inhibitor (ciclosporin or tacrolimus), an antiprolif - erative agent (azathioprine or mycophenolic acid) and steroids.