Tumor necrosis factor receptor superfamily member 27, also known as X-linked ectodysplasin-A2 receptor, EDA-A2 receptor, EDA2R, XEDAR and TNFRSF27, is a single-pass type III membrane protein. TNFRSF27 / EDA2R contains threeTNFR-Cys repeats. It is a new member of the tumor necrosis factor receptor family that has been shown to be highly expressed in ectodermal derivatives during embryonic development and binds to ectodysplasin-A2 (EDA-A2). TNFRSF27 / EDA2R is a receptor for EDA isoform A2, but not for EDA isoform A1. TNFRSF27 / EDA2R mediates the activation of the NF-kappa-B and JNK pathways. The activation seems to be mediated by binding to TRAF3 and TRAF6. Ectodysplasin, a member of the tumor necrosis factor family, is encoded by the anhidrotic ectodermal dysplasia EDA gene. Mutations in EDA give rise to a clinical syndrome characterized by loss of hair, sweat glands, and teeth. EDA-A1 and EDA-A2 are two isoforms of ectodysplasin that differ only by an insertion of two amino acids. This insertion functions to determine receptor binding specificity, such that EDA-A1 binds only the receptor EDAR, whereas EDA-A2 binds only the related, but distinct, X-linked ectodysplasin-A2 receptor (XEDAR).
Angiopoietin-2 (Ang-2; also ANGPT2) is a secreted glycoprotein that plays a complex role in angiogenesis and inflammation. Both Ang-2 and the related Angiopoietin-1 (Ang-1) are ligands for the receptor tyrosine kinase Tie-2. While Ang-1 is a potent Tie 2 agonist, Ang-2 may act as either a Tie-2 antagonist or agonist, depending upon its state of multimerization. The higher the order of oligomer, the more effective Ang-2 becomes as a Tie-2 agonist. The short isoform appears to block the binding of either Ang-1 or full-length Ang-2 to Tie-2. Ang-2 functions as a pro-angiogenic factor, although it can also induce EC death and vessel regression. Upon its release from quiescent EC, it regulates vascular remodeling by promoting EC survival, proliferation, and migration and destabilizing the interaction between EC and perivascular cells. In addition, ANG-2 is strongly expressed in the vasculature of many tumors and it has been suggested that ANG-2 may act synergistically with other cytokines such as vascular endothelial growth factor to promote tumor-associated Angiogenesis and tumor progression.
Angiotensin-Converting Enzyme 2 (ACE-2) is an integral membrane protein and a zinc metalloprotease of the ACE family, the ACE family includes somatic and germinal ACE. ACE-2 cleaves angiotensins I and II as a carboxypeptidase, ACE-2 converts angiotensin I to angiotensin 1-9, and angiotensin II to angiotensin 1-7. ACE-2 is also able to hydrolyze apelin-13 and dynorphin-13 with high efficiency. ACE-2 can be high expressed in testis, kidney and heart, in colon, small intestine and ovary at moderate levels. Captopril and lisinopril as the classical ACE inhibitor don’t inhibit ACE-2 activity. ACE-2 may play an important role in regulating the heart function.
T-lymphocyte activation antigen CD86 (B7-2) is a glycosylated protein in the B7 family. B7 family members are transmembrane cell surface molecules that play important roles in immune activation and the maintenance of immune tolerance. It is highly expressed on activated antigen presenting cells. CD86 involved in the costimulatory signal essential for T-lymphocyte proliferation and interleukin-2 production, by binding CD28 or CTLA-4. It may play a critical role in the early events of T-cell activation and costimulation of naive T-cells, such as deciding between immunity and anergy that is made by T-cells within 24 hours after activation. It is expressed by activated B-lymphocytes and monocytes and promoted by MARCH8 and results in endocytosis and lysosomal degradation.
B7 Homolog 4 (B7-H4) is glycosylated member of the B7 family of immune costimulatory proteins.It is widely expressed, including in kidney, liver, lung, pancreas, placenta, prostate, spleen, testis and thymus. B7-H4 negatively regulates T-cell-mediated immune response by inhibiting T-cell activation, proliferation, cytokine production and development of cytotoxicity. When expressed on the cell surface of tumor macrophages, plays an important role, together with regulatory T-cells (Treg), in the suppression of tumor-associated antigen-specific T-cell immunity. It also involved in promoting epithelial cell transformation.
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