Antigen-presenting cell receptors and processing pathways for birch pollen allergoid

This target refers to the group of receptors and intracellular pathways on antigen-presenting cells (APCs), such as dendritic cells and monocytes, that mediate the recognition and internalization of birch pollen allergoids (Sirvent et al., 2016). Allergoids are chemically modified allergens, typically polymerized with glutaraldehyde, designed to reduce IgE binding while maintaining T-cell immunogenicity for use in allergen immunotherapy (AIT) (Pfaar et al., 2022). Research has identified Scavenger Receptor Class A (SR-A/CD204) and Mannose Receptor (MR/CD206) as the primary receptors responsible for the efficient uptake of these allergoids compared to native allergens (Sirvent et al., 2016). Once internalized, the allergoids enter the endolysosomal processing pathway, where they are degraded into peptides for presentation on MHC class II molecules (Sirvent et al., 2016). This specific recognition and processing route leads to a modulation of the immune response, favoring the induction of regulatory T cells (Tregs) and the production of anti-inflammatory cytokines like IL-10 (Biedermann et al., 2019). Clinically, this mechanism is exploited in AIT to shift the immune system away from a Th2-mediated allergic response toward a tolerant state (Pfaar et al., 2022). The interaction between allergoids and these APC receptors results in the production of protective IgG4 antibodies, which block IgE-mediated mast cell degranulation (Sirvent et al., 2016). Understanding these pathways is essential for optimizing the design of next-generation vaccines, such as mannan-conjugated allergoids (T502), for birch pollen allergy (Pfaar et al., 2022).

Other names

APC receptors for birch pollen allergoidScavenger receptor class A (SR-A)Mannose receptor (MR)CD204CD206Bet v 1 allergoid uptake pathway

Allergoids are internalized by antigen-presenting cells via scavenger and mannose receptors, leading to altered endolysosomal processing and presentation that induces regulatory T-cell responses and IgG4 production (Sirvent et al., 2016; Pfaar et al., 2022).