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Department of Experimental Immunology and Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Institute of Development, Aging and Cancer, Tohoku University, Aoba-ku, Sendai-shi 980-8575, Japan

CORRESPONDENCE Toshiyuki Takai: tostakai{at}idac.tohoku.ac.jp

Allergy is caused by immune effector cells, including mast cells and basophils. Cellular signaling that activates these effector cells is regulated by different inhibitory receptors on their surface. We show that human leukocyte immunoglobulin (Ig)-like receptor (LILR) B2 and its mouse orthologue, paired Ig-like receptor (PIR)–B, constitutively associate to major histocompatibility complex (MHC) class I on the same cell surface (in cis). The IgE-mediated effector responses were augmented in ß₂-microglobulin (ß₂m) and PIR-B–deficient mast cells. In addition, the increased cytokine production of ß₂m-deficient mast cells was not affected by the co-culture with MHC class I–positive mast cells, showing that less cis interaction between PIR-B and MHC class I on mast cells led to the increased cytokine release. Thus, the constitutive cis binding between LILRB2 or PIR-B and MHC class I has an essential role in regulating allergic responses.

Abbreviations used: BMMC, bone marrow–derived mast cell; ß₂m, ß₂-microglobulin; FcRI, high affinity FcR for IgE; FcRIIB and FcRIII, type IIB and type III, respectively, low affinity FcR for IgG; FRET, fluorescence resonance energy transfer; HRP, horseradish peroxidase; ITAM, immunoreceptor tyrosine–based activation motif; ITIM, immunoreceptor tyrosine–based inhibition motif; LILR, leukocyte Ig-like receptor; MIP, macrophage inflammatory protein; PIR, paired Ig-like receptor; PLC, phospholipase C; PMT, photomultiplier; SHP, Src homology domain 2–containing tyrosine phosphate; SIRP, signal regulatory protein.

A. Masuda and A. Nakamura contributed equally to this work.

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