B7-1 and B7-2 co-stimulatory molecules (CD80 (for B7-1), CD86 (for B7-2))

B7-1 (CD80) and B7-2 (CD86) are homologous type I transmembrane glycoproteins belonging to the immunoglobulin superfamily, expressed predominantly on the surface of antigen-presenting cells such as dendritic cells, macrophages, and B cells[1][2]. These molecules serve as co-stimulatory ligands necessary for full T cell activation, acting by binding to CD28 and CTLA-4 receptors on T cells. B7-1 and B7-2 have partially redundant but distinct roles: B7-2 is constitutively expressed and rapidly upregulated upon immune activation, facilitating early T cell priming, whereas B7-1 expression is induced later and may play a larger role in the regulation and amplification of T cell activity in peripheral tissues[1][2]. Functionally, their engagement influences T cell differentiation (Th1/Th2 balance) and B cell antibody class switching, as well as the strength and character of immune responses. Their interaction is a central therapeutic target in autoimmunity, transplant rejection, and cancer immunotherapy, as modulating these co-stimulatory signals can tune immune activation or tolerance[1][2].

Other names

B7-1: CD80B7-2: CD86B7 family co-stimulatory ligandsCluster of Differentiation 80 (CD80)Cluster of Differentiation 86 (CD86)B7-1 antigenB7-2 antigen

Inhibition of B7-1/CD80 or B7-2/CD86 interaction with CD28 or CTLA-4 to modulate T cell co-stimulation and immune activation Fusion proteins (e.g., abatacept, belatacept) bind B7-1 or B7-2, preventing native receptor binding and dampening T cell responses