Intravenously administered glucocorticoids , such as prednisone , are the standard of care in acute GvHD  and chronic GVHD.  The use of these glucocorticoids is designed to suppress the T-cell-mediated immune onslaught on the host tissues; however, in high doses, this immune-suppression raises the risk of infections and cancer relapse. Therefore, it is desirable to taper off the post-transplant high-level steroid doses to lower levels, at which point the appearance of mild GVHD may be welcome, especially in HLA mis-matched patients, as it is typically associated with a graft-versus-tumor effect. [ citation needed ] . Cyclosporine and tacrolimus are inhibitors of calcineurin. Both substances are structurally different but have the same mechanism of action. Cyclosporin binds to the cytosolic protein Peptidyl-prolyl cis-trans isomerase A (known as cyclophilin), while tacrolimus binds to the cytosolic protein Peptidyl-prolyl cis-trans isomerase FKBP12. These complexes inhibit calcineurin, block dephosphorylation of the transcription factor NFAT of activated T-cells and its translocation into the nucleus.  Standard prophylaxis involves the use of cyclosporine for six months with methotrexate. Cyclosporin levels should be maintained above 200 ng/ml.  Other substances that have been studied for GvHD prophylaxis include, for example: sirolimus, pentostatin and alemtuzamab. 
Immunosuppressive therapy is used to treat acute GVHD. These drugs counter the attacks by the graft T-cells, which view the host cells as foreign. The patient may need to take corticosteroids, such as prednisolone. Steroids are used to try to help bring the patient’s immune system back into control and minimise inflammation. However, steroids can cause side effects such as higher levels of blood sugar, fluid retention, mood problems, a greater appetite and stomach pain. Long-terms use of steroids has been linked to diabetes , muscle weakness, infections and cancers.