Editing Immune system (section)

=== Immunosuppression ===
[[Immunosuppressive drug]]s are used to control autoimmune disorders or [[inflammation]] when excessive tissue damage occurs, and to prevent rejection after an [[organ transplant]].{{sfn|Ciccone |2015 |loc = Chapter [https://books.google.com/books?id=Te1vCAAAQBAJ&q=%22immunosuppressive+drugs%22+autoimmune+tissue+damage&pg=PA625 37]}}<ref name= Taylor>{{cite journal | vauthors = Taylor AL, Watson CJ, Bradley JA | title = Immunosuppressive agents in solid organ transplantation: Mechanisms of action and therapeutic efficacy | journal = Critical Reviews in Oncology/Hematology | volume = 56 | issue = 1 | pages = 23–46 | date = Oct 2005 | pmid = 16039869 | doi = 10.1016/j.critrevonc.2005.03.012 }}</ref>

[[Anti-inflammatory]] drugs are often used to control the effects of inflammation. [[Glucocorticoid]]s are the most powerful of these drugs and can have many undesirable [[adverse effect|side effects]], such as [[central obesity]], [[hyperglycemia]], and [[osteoporosis]].<ref>{{cite journal | vauthors = Barnes PJ | title = Corticosteroids: the drugs to beat | journal = European Journal of Pharmacology | volume = 533 | issue = 1–3 | pages = 2–14 | date = Mar 2006 | pmid = 16436275 | doi = 10.1016/j.ejphar.2005.12.052 }}</ref> Their use is tightly controlled. Lower doses of anti-inflammatory drugs are often used in conjunction with cytotoxic or immunosuppressive drugs such as [[methotrexate]] or [[azathioprine]].

[[Chemotherapy|Cytotoxic drugs]] inhibit the immune response by killing dividing cells such as activated T cells. This killing is indiscriminate and other [[constantly dividing cells]] and their organs are affected, which causes toxic side effects.<ref name= Taylor /> Immunosuppressive drugs such as [[cyclosporin]] prevent T cells from responding to signals correctly by inhibiting [[signal transduction]] pathways.<ref>{{cite journal | vauthors = Masri MA | title = The mosaic of immunosuppressive drugs | journal = Molecular Immunology | volume = 39 | issue = 17–18 | pages = 1073–77 | date = Jul 2003 | pmid = 12835079 | doi = 10.1016/S0161-5890(03)00075-0 }}</ref>