The cell surface glycoprotein B7-2, also known as cluster of differentiation 86 (CD86), belongs to the B7 family of co-stimulatory molecules, which are expressed on antigen-presenting cells (APCs), including dendritic cells, macrophages and B cells. Resting APCs express low levels of B7 molecules, but various stimuli, such as microbial products and cytokines produced during innate immune reactions against pathogens, induce an increased expression of B7 molecules in order to promote adaptive immune responses. This regulated expression ensures that T cells are activated only when needed. When T cells encounter antigens displayed by APCs, which is the first signal required for complete T cell activation, B7-2 interacts with CD28 providing a co-stimulatory signal, the second crucial signal. T cell activation leads to cytokine production and proliferation of T cells as well as differentiation into effector and memory T cells. This interaction is counterbalanced by the cytotoxic T lymphocyte antigen-4 (CTLA-4), which is expressed on T cells after antigen recognition and has a higher affinity for B7-2 than CD28. CTLA-4 provides inhibitory signals leading to downregulation of immune responses. Dysregulation of B7-2 causes autoimmune diseases, inflammatory disorders and cancer. Therefore, therapeutic strategies targeting B7-2 or its interactions are being explored to dampen autoimmune diseases and to enhance anti-cancer immunity.
