In the thymus, the<unk>  causes transcription of a wide selection of organ-specific genes that create proteins that are usually only expressed in peripheral tissues, creating an "immunological self-shadow" in the thymus. It is important that self-reactive T cells that bind strongly to self-antigen are eliminated in the thymus (via the process of negative selection), otherwise they may later encounter and bind to their corresponding self-antigens and initiate an<unk>  reaction. So the expression of non-local proteins by<unk>  in the thymus reduces the threat of<unk> ty by promoting the elimination of auto-reactive T cells that bind antigens not normally found in the thymus. Furthermore, it has been found that<unk>  is expressed in a population of stromal cells located in secondary lymphoid tissues, however these cells appear to express a distinct set of TRAs compared to mTECs. Research in knockout mice has demonstrated that<unk>  functions through initiating the transcription of a diverse set of self-antigens, such as insulin, in the thymus. This expression then allows maturing thymocytes to become tolerant towards peripheral organs, thereby suppressing<unk>  disease. The<unk>  gene is expressed in many other tissues as well.<unk>  gene is also expressed in the 33D1+ subset of dendritic cells in mouse and in human dendritic cells.
Autoimmune regulator
Inflammatory cytokine
Lymphokine
Tumor antigen
Cytokine
Bacterial adhesin
Autoantibody
Microantibody