CD300f is a potential therapeutic target for the treatment of food allergy.

The interaction between CD300f and its ligand ceramide suppresses IgE-mediated mast cell activation and anaphylactic responses through phosphorylation of immunoreceptor tyrosine-based inhibitory and switch motifs.[2] CD300f also regulates gut inflammation by different mechanisms.[[3]] Nevertheless, it remains unknown whether CD300f regulates the development of food allergy. Serum levels of total IgE (C), OVA-specific IgE (D) and MCPT-1 (E), and the numbers of jejunum mast cells (F) in WT and CD300f-/- (KO) mice after the last challenge. According to numerous studies, Tregs inhibit both Th2 skewing, involving food antigen-specific IgE production and IL-9-mediated mast cell hyperplasia, and IgE/antigen-mediated mast cell activation, which are pivotal in the development of food allergy, whereas Th2- and mast cell-derived cytokines (eg, IL-4) downregulate Tregs.[[1], [6], [9]] Accordingly, CD300f in intestinal mast cells (possibly in concert with CD103 SP + sp CD11b SP + sp cells) inhibits the development of OVA-induced food allergy by suppressing mast cell activation with the skewing of Th2/Treg balance toward Th2. [Extracted from the article]