Sputum basophils from allergic asthmatic patients do not express IL‐7Rα that is essential for TSLP signalling

Abstract

AbstractBasophils are crucial in regulating allergic reactions via immediate secretion of multiple mediators upon IgE‐induced degranulation. IL‐3 regulates the development and activation of human basophils while epithelial cytokine thymic stromal lymphopoietin (TSLP) is another key regulator for murine basophils. Despite association of increased TSLP with exaggerated basophil responses in oesophageal biopsies, the effects of TSLP in regulating human basophil degranulation and activation are under debate. In this study, we aimed to examine whether human basophils responded to TSLP by co‐expression of TSLP receptors, TSLPR and IL‐7Rα (CD127), upon in vitro activation and in sputum of allergic asthmatic patients. Flow cytometric analysis of fresh basophils from healthy controls revealed no detectable TSLPR and CD127. Further flow cytometric analysis of basophils from healthy controls in vitro stimulated by multiple established basophil modulators for 24 hours showed induction of TSLPR but not CD127 by IL‐3 (10 ng/ml), anti‐IgE (10 μg/ml) and C5a (50 ng/ml). One‐hour stimulation of basophils from allergic asthmatic patients and healthy controls by TSLP (50 ng/ml) with or without IL‐3 (10 ng/ml) and anti‐IgE (10 μg/ml) had no effect on induction of CD63+ degranulated basophils. Similarly, TSLP (50 ng/ml) with or without IL‐3 (10 ng/ml) and anti‐IgE (10 μg/ml) did not induce IL‐4 and IL‐13 production by basophils from healthy controls. Further ex vivo analysis revealed that sputum basophils from allergic asthmatic patients did not express CD127. We conclude that human basophils from healthy controls and allergic asthmatic patients do not respond to TSLP as lacking CD127.