Low-affinity Fc gamma receptor (FcγRII and FcγRIII) (FcγR)

Antigen-presenting cell receptors, primarily the low-affinity Fc gamma receptors (FcγRII/CD32 and FcγRIII/CD16), are the key molecules responsible for the uptake and processing of Human Papillomavirus (HPV) L1 virus-like particles (VLPs) by dendritic cells and macrophages. These receptors facilitate the internalization of VLPs from high-risk HPV types, such as HPV16, 18, 33, and 58, which are the primary antigens in prophylactic HPV vaccines like Gardasil 9. A distinctive feature of HPV VLPs is their ability to bind directly to these receptors on immature antigen-presenting cells (APCs) even in the absence of specific antibodies, an interaction that serves as an intrinsic adjuvant by inducing APC maturation. This process involves the upregulation of co-stimulatory molecules and the secretion of pro-inflammatory cytokines, which are essential for the subsequent activation of T cells and the generation of a robust, long-lasting humoral immune response. Consequently, these receptors are fundamental to the high efficacy of current HPV vaccines in preventing cervical cancer and other HPV-associated malignancies. Beyond Fc gamma receptors, other molecules such as heparan sulfate proteoglycans and C-type lectin receptors (e.g., DC-SIGN) may also contribute to the initial attachment and uptake of VLPs. Understanding the precise interaction between VLPs and these receptors is vital for the development of next-generation vaccines with broader coverage or improved delivery methods.

Other names

CD16CD32Fc gamma receptor IIFc gamma receptor IIIFcgammaRIIFcgammaRIIIAntigen-presenting cell receptors for HPV L1 VLPsCD16aCD16bCD32aCD32bCD32c

Binding of HPV L1 virus-like particles (VLPs) to Fc gamma receptors (FcγRII and FcγRIII) on antigen-presenting cells (APCs) triggers their internalization and processing, leading to APC maturation and the presentation of viral antigens to T cells, which initiates a robust adaptive immune response.