B7-2/CD86 Protein

Angiopoietin-1 (ANG-1) is a secreted glycoprotein that plays a critical role in the development and maintenance of the vascular system. It contains a N-terminal coiled-coil region and a C-terminal fibrinogen-like domain separated by a short flexible region. Angiopoietin-1 binds and activates the receptor tyrosine kinase Tie-2, and its association into tetramers is important for full Tie-2 activation. Angiopoietin-1 ligation of Tie-2 on vascular endothelial cells (EC) induces the development and branching of blood vessels. In confluent EC (i.e. in homeostasis), multimeric Angiopoietin-1 enhances vascular integrity by promoting the in trans homotypic association of Tie-2 between EC or with the substratum. In addition, Angiopoietin-1 suppresses several VEGF-induced effects on the vasculature including endothelial permeability, stretch-induced release of Angiopoietin-2, and up-regulation of the leukocyte adhesion molecules VCAM-1, ICAM-1, and E-Selectin. Angiopoietin-1 also interacts with a variety of integrins and the extracellular matrix independently of Tie-2. These interactions support the adhesion, migration and stress resistance of EC, fibroblasts, and myocytes. Angiopoietin-1 can protect against pulmonary arterial hypertension, reduce the extent of fibrosis and remodeling in infarcted diabetic myocardium, and enhance tumor progression and metastasis.CD86 is a well-known costimulatory molecule in its interaction with CD28 and/or CTLA present on T cells, and is essential for full activation of naive T-cell and subsequent differentiation. Usually, the B7 molecules are expressed mainly on APCs and B cells and in specific conditions on other activated cells. These costimulatory molecules are involved in the development of allergic inflammation and airways hyperreactivity (AHR) in allergen-challenged mice. Activated T cells, CD4+CD25+, express CD86 in the first 60 minutes after the specific inhalation exposure. These T cells can be relevant in IgE mediated allergic reaction possibly by an autocrine co-stimulation via CD28/CTLA activation pathway. The blockage of the expression of CD86 could be a potential therapeutical target to reduce the magnitude or the progression of the allergic reaction.