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J. Exp. Med.,
Volume 189, Number 4, February 15, 1999 673-682
By
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.
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