The anti‐FcεRI antibody MAR‐1 depletes basophils and cross‐reacts with myeloid cells through its Fc portion

International audience; In humans, the high-affinity IgE receptor FcεRI is expressed as a tetramer in mast cells (MCs) and basophils, and as a trimer in additional myeloid cell populations, including monocytes, macrophages, dendritic cells (DCs), and Langerhans cells.1 In mice, the expression profile of FcεRI is more debatable. Some studies report FcεRI+ macrophages and DCs.2 However, recent data indicate that the anti-FcεRI mAb (clone MAR-1) used in all these studies can recognize myeloid cells in an FcεRI-independent manner, and cross-reacts with FcγRI and FcγRIV.3, 4 Since MAR-1 has been extensively used in vivo to assess the role of FcεRI and to deplete basophils,5 the off-target effects of this mAb raise concerns regarding some of the conclusions made in prior studies. We thus decided to assess by which mechanism MAR-1 cross-reacts with FcγRs, and whether this cross-reactivity accounts for some of the functions previously attributed to FcεRI and/or basophils.