CD300a is expressed on human basophils and seems to inhibit IgE/FcεRI-dependent anaphylactic degranulation.

The final response that leads to basophil degranulation results from a cross-talk between activatory and inhibitory signals. However, in the context of basophil biology, the inhibitory mechanisms that control these processes are still poorly understood. To investigate the expression and function of the inhibitory receptor CD300a in human basophils. Peripheral blood of 20 patients with birch pollen allergy and 10 healthy control individuals were assessed for CD300a expression before and after activation. To study the function of CD300a, basophils were pre-incubated with anti-human CD300a/c monoclonal antibodies and analyzed for the up-regulation of the activation marker CD203c and appearance of the degranulation marker CD63 following IgE-dependent and IgE-independent triggering. Basophils from allergic individuals constitutively expressed significantly less CD300a than non-allergics (P = 0.001). However, after cross-linking with either anti-IgE or recombinant major birch pollen allergen (rBet v 1), basophils from allergic patients demonstrated a significant and rapid (3 min) up-regulation of CD300a expression in all activated basophils that persisted for over 2 h (P < 0.05). Moreover, CD300a expression was significantly higher in the CD203c(bright+) CD63(bright+) subpopulation than in CD203c(bright+) CD63(-) cells (P < 0.05). In both patients and controls, pre-incubation with anti-CD300a/c significantly inhibited IgE-mediated CD63 expression (P < 0.05), though it did not affect CD203c. In contrast, IgE-independent basophil activation was not inhibited by CD300a/c engagement. CD300a is expressed on human peripheral blood basophils and rapidly up-regulated upon cross-linking of IgE/FcεRI and suppresses anaphylactic degranulation.