CD352. also known as SLAMF6 or NTB-A, is a cell surface glycoprotein belonging to the signaling lymphocytic activation molecule (SLAM) family. It functions as a self-ligand receptor expressed on various immune cells, including T cells, natural killer (NK) cells, B cells, and dendritic cells. Structurally, CD352 contains immunoglobulin-like domains, a transmembrane region, and cytoplasmic tyrosine-based signaling motifs (ITSMs) that recruit phosphatases like SHP-1/2 or adaptor proteins to modulate immune responses.
CD352 plays dual roles in immune regulation, acting as a co-stimulatory or co-inhibitory molecule depending on cellular context. It facilitates cell-cell interactions, particularly in lymphocyte activation, adhesion, and cytotoxicity. In T cells, CD352 engagement fine-tunes T-cell receptor (TCR) signaling, impacting effector functions and exhaustion. Studies highlight its involvement in chronic viral infections (e.g., HIV, HCV) and cancer, where sustained CD352 expression correlates with T-cell dysfunction.
Antibodies targeting CD352 are research tools or potential therapeutics. Blocking CD352 may restore anti-tumor immunity or mitigate autoimmune reactions by altering signaling pathways. Conversely, agonist antibodies might enhance immune activation in specific contexts. Its role as a biomarker for immune cell states (e.g., exhausted T cells) further underscores clinical relevance. Research continues to explore CD352's mechanistic nuances and therapeutic targeting in immunotherapy and immune-related disorders.