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From the Department of Molecular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan

Histamine is considered one of the important mediators of immediate hypersensitivity and inflammation, and acts via G protein–coupled receptors. Here, we report that histamine may affect antigen receptor–mediated immune responses of T and B cells via a signal(s) from histamine H1 receptors (H1Rs). Histamine exhibited enhancing effects on the in vitro proliferative responses of anti-CD3– or anti-IgM–stimulated spleen T and B cells, respectively, at the culture condition that the fetal calf serum was dialyzed before culture and c-kit–positive cells were depleted from the spleen cells. In studies of histamine H1R knockout mice, H1R-deficient T cells had low proliferative responses to anti-CD3 cross-linking or antigen stimulation in vitro. B cells from H1R-deficient mice were also affected, demonstrating low proliferative responses to B cell receptor cross-linking. Antibody production against trinitrophenyl-Ficoll was reduced in H1R-deficient mice. Other aspects of T and B cell function were normal in the H1R knockout mice. H1R-deficient T and B cells showed normal responses upon stimulation with interleukin (IL)-2, IL-4, CD40 ligand, CD40 ligand plus IL-4, and lipopolysaccharide. Collectively, these results imply that the signal generated by histamine through H1R augments antigen receptor–mediated immune responses, suggesting cross-talk between G protein–coupled receptors and antigen receptor–mediated signaling.

Key Words: G protein • antigen receptor • signaling • histamine H1 receptor • G protein– coupled receptor

We express our sincere thanks to Dr. Peter Burrows for reading the manuscript and for his helpful comments. We also thank Dr. M. Nakashima for his invaluable assistance with the experiments.

¹ Abbreviations used in this paper: BCR, B cell receptor; Btk, Bruton's tyrosine kinase; GPCR, G protein–coupled receptor; G protein, guanine-nucleotide binding protein; HRP, horseradish peroxidase; MAPK, mitogen-activated protein kinase; PLC, phospholipase C; PTK, protein tyrosine kinases; TMB, tetramethylbenzidine.

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