Cd86, also known as B7-2, is a costimulatory molecule that plays a crucial role in the immune system. It interacts with CD28 and CTLA-4 present on T cells, which is essential for the full activation of naïve T-cells and their subsequent differentiation. This interaction is involved in pathways regulating T cell immunity, balancing activation and inhibition of T cell responses [1,2,3,4].

CTLA-4 can capture CD86 from antigen-presenting cells via trans-endocytosis, leading to the degradation of this costimulatory ligand and impaired costimulation via CD28 [2]. Mutations that disrupt CD86 trans-endocytosis can cause autoimmune diseases, indicating a link between defects in this process and autoimmunity [1].

In the context of regulatory T cells (Tregs), CD86 is the dominant ligand for Treg proliferation, survival, and maintenance of a regulatory phenotype, despite its lower affinity for CD28, as CD80-CD28 interactions are selectively impaired by high levels of CTLA-4 [6].

Low CD86 expression in exfoliated cervical cells can predict histological complete response after administration of the therapeutic human papillomavirus vaccine IGMKK16E7 [5].

In conclusion, Cd86 is essential for T cell-mediated immune responses. Research on Cd86, especially through models like CTLA-4-mediated trans-endocytosis studies, has provided insights into its role in autoimmunity and as a biomarker in vaccine response. Understanding Cd86 is crucial for comprehending immune regulation and developing treatments related to immune-mediated diseases and vaccines.