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Human Basophils Express the Glycosylphosphatidylinositol-Anchored Low-Affinity IgG Receptor FcRIIIB (CD16B)¹

Nihad Meknache^2,*,, Friederike Jönsson^2,*,, Jérôme Laurent, Marie-Thérèse Guinnepain and Marc Daëron^3,*,

^* Institut Pasteur, Département d’Immunologie, Unité d’Allergologie Moléculaire et Cellulaire, Paris; Institut National de la Santé et de la Recherche Médicale, Unité 760, Paris; and Consultation d’Allergologie, Centre Médical de l’Institut Pasteur, Paris, France

Basophils express not only high-affinity IgE receptors, but also low-affinity IgG receptors. Which, among these receptors, are expressed by human basophils is poorly known. Low-affinity IgG receptors comprise CD32 (FcRIIA, FcRIIB, and FcRIIC) and CD16 (FcRIIIA and FcRIIIB). FcRIIA, FcRIIC, and FcRIIIA are activating receptors, FcRIIB are inhibitory receptors, FcRIIIB are GPI-anchored receptors whose function is poorly understood. Basophils were reported to express FcRII, but not FcRIII. We aimed at further identifying basophil IgG receptors. Basophils from normal donors and from patients suffering from an allergic skin disease (atopic dermatitis), allergic respiratory diseases (allergic rhinitis and asthma), or a nonallergic skin disease (chronic urticaria) were examined. We found that normal basophils contain FcRIII transcripts and express FcRIIIB, but not FcRIIIA, which were detected on 24–81% basophils from normal donors and on 12–100% basophils from patients. Noticeably, the proportion of FcRIIIB⁺ basophils was significantly lower in atopic dermatitis patients than in other subjects. This decreased FcRIII expression was not correlated with an activated phenotype of basophils in atopic dermatitis patients, although FcRIIIB expression was down-regulated upon basophil activation by anti-IgE. Our results challenge the two dogmas 1) that basophils do not express FcRIII and 2) that FcRIIIB is exclusively expressed by neutrophils. They suggest that a proportion of basophils may be lost during enrichment procedures in which FcRIII⁺ cells are discarded by negative sorting using anti-CD16 Abs. They unravel an unexpected complexity of IgG receptors susceptible to modulate basophil activation. They identify a novel systemic alteration in atopic dermatitis.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by the Institut Pasteur, the Institut National de la Santé et de la Recherche Médicale, the Agence Nationale pour la Recherche, and the Fondation pour la Recherche Médicale Program Défis de la Recherche en Allergologie. N.M. was financially supported by the Fondation pour la Recherche Médicale and the Institut Pasteur; F.J. was financially supported by the Agence Nationale pour la Recherche.

² N.M. and F.J. contributed equally.

³ Address correspondence and reprint requests to Dr. Marc Daëron, Unité d’Allergologie Moléculaire et Cellulaire, Bâtiment Metchnikoff, Institut Pasteur, 25 rue du Docteur Roux, 75015 Paris, France. E-mail address: daeron{at}pasteur.fr

⁴ Abbreviations used in this paper: RAM, rabbit anti-mouse Ig; MFI, mean fluorescence intensity; PI-PLC, phosphatidylinositol-specific phospholipase C; CHO, Chinese hamster ovary; SSC, side scatter; FSC, forward scatter.