L-Asparaginase (L-ASP) derived from E. coli is a key drug in the treatment of childhood acute lymphoblastic leukemia (ALL). L-Asp often causes hypersensitivity reactions, including anaphylaxis. We reported that a neutralizing antibody (Ab) of IgE was effective to inhibit L-ASP-induced allergy in the mouse model. In the present study, we used RBL-2H3 cells to establish in vitro model of L-ASP allergy.
Male BALB/c mice were sensitized by L-ASP with Al(OH)3 on days 0 and 14. Cyclophosphamide (CY) was i.p. administrated on days –2 and 12. The serum was collected on day 26. Total IgE level in the serum was measured by ELISA. RBL-2H3 was sensitized by the serum and stimulated by L-ASP to determine β-hexosaminidase (β-Hex) release in vitro.
L-ASP sensitization increased serum IgE level, which was enhanced by CY at 150 mg/kg. When RBL-2H3 was sensitized by L-ASP-sensitized serum in vitro, L-ASP stimulated β-Hex release from the cells. The serum of CY-treated mice induced higher β-Hex release than normal. Anti-IgE Ab inhibited allergic β-Hex release both in vitro and ex vivo.
From the present results, L-ASP sensitization induced IgE production in vivo and this serum induced β-Hex release from RBL-2H3 cells. Using cell lines expressing FceRI, it can be possible to evaluate L-ASP allergy and efficacy of anti-IgE Ab in vitro.

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