Editing Bcl-2 (section)

===Auto-immune diseases===
[[Apoptosis]] plays an active role in regulating the immune system. When it is functional, it can cause immune unresponsiveness to self-[[antigens]] via both central and peripheral tolerance. In the case of defective apoptosis, it may contribute to etiological aspects of autoimmune diseases.<ref name="pmid17162368">{{cite journal | vauthors = Li A, Ojogho O, Escher A | title = Saving death: apoptosis for intervention in transplantation and autoimmunity | journal = Clinical & Developmental Immunology | volume = 13 | issue = 2–4 | pages = 273–282 | year = 2006 | pmid = 17162368 | pmc = 2270759 | doi = 10.1080/17402520600834704 }}</ref> The autoimmune disease [[Diabetes mellitus type 1|type 1 diabetes]] can be caused by defective apoptosis, which leads to aberrant T cell [[Activation-induced cytidine deaminase|AICD]] and defective peripheral tolerance. Due to the fact that [[dendritic cell]]s are the immune system's most important [[antigen-presenting cell]]s, their activity must be tightly regulated by mechanisms such as apoptosis. Researchers have found that mice containing dendritic cells that are [[BCL2L11|Bim]] -/-, thus unable to induce effective apoptosis, have [[autoimmune disease]]s more so than those that have normal dendritic cells.<ref name="pmid17162368"/> Other studies have shown that dendritic cell lifespan may be partly controlled by a timer dependent on anti-apoptotic Bcl-2.<ref name="pmid17162368"/>