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J. Exp. Med., Volume 189, Number 2, January 18, 1999 309-318

Biochemical Nature and Cellular Distribution of the Paired Immunoglobulin-like Receptors, PIR-A and PIR-B

By Hiromi Kubagawa,* Ching-Cheng Chen,Dagger Le Hong Ho, Toshihide Shimada,parallel Lanier Gartland, Charles Mashburn, Takahiro Uehara,parallel Jeffrey V. Ravetch,** and Max D. CooperDagger §parallel

From the Division of Developmental and Clinical Immunology, * Department of Pathology, Dagger  Department of Microbiology, § Department of Pediatrics, and parallel  Department of Medicine, University of Alabama at Birmingham, and the  Howard Hughes Medical Institute, Birmingham, Alabama 35294; and the ** Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York 10021

PIR-A and PIR-B, paired immunoglobulin-like receptors encoded, respectively, by multiple Pira genes and a single Pirb gene in mice, are relatives of the human natural killer (NK) and Fc receptors. Monoclonal and polyclonal antibodies produced against a recombinant PIR protein identified cell surface glycoproteins of ~85 and ~120 kD on B cells, granulocytes, and macrophages. A disulfide-linked homodimer associated with the cell surface PIR molecules was identified as the Fc receptor common gamma  (FcRgamma c) chain. Whereas PIR-B fibroblast transfectants expressed cell surface molecules of ~120 kD, PIR-A transfectants expressed the ~85-kD molecules exclusively intracellularly; PIR-A and FcRgamma c cotransfectants expressed the PIR-A/ FcRgamma c complex on their cell surface. Correspondingly, PIR-B was normally expressed on the cell surface of splenocytes from FcRgamma c-/- mice whereas PIR-A was not. Cell surface levels of PIR molecules on myeloid and B lineage cells increased with cellular differentiation and activation. Dendritic cells, monocytes/macrophages, and mast cells expressed the PIR molecules in varying levels, but T cells and NK cells did not. These experiments define the coordinate cellular expression of PIR-B, an inhibitory receptor, and PIR-A, an activating receptor; demonstrate the requirement of FcRgamma c chain association for cell surface PIR-A expression; and suggest that the level of FcRgamma c chain expression could differentially affect the PIR-A/PIR-B equilibrium in different cell lineages.

Key words: Fc receptor gamma  chain;  activating receptor;  inhibitory receptor;  dendritic cells;  innate immunity


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