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A Role for B Cell-Activating Factor of the TNF Family in Chemically Induced Autoimmunity¹

Yan Zheng^*, Stefania Gallucci, John P. Gaughan, Jane A. Gross and Marc Monestier^2,*

^* Department of Microbiology and Immunology, and Department of Biostatistics, Temple University School of Medicine, Philadelphia, PA 19140; Division of Rheumatology, Joseph Jr. Strokes Research Institute, The Children’s Hospital of Philadelphia, Philadelphia, PA 19104; and Department of Immunology, ZymoGenetics, Seattle, WA 98102

After exposure to subtoxic doses of heavy metals such as mercury, H-2^s mice develop an autoimmune syndrome consisting of the rapid production of IgG autoantibodies that are highly specific for nucleolar autoantigens and a polyclonal increase in serum IgG1 and IgE. In this study, we observe that HgCl₂ administration in susceptible mice results in the elevated production of B cell-activating factor of the TNF family ((BAFF) also known as BLyS, TALL-1, zTNF-4, THANK, and TNSF13B), a B cell growth factor belonging to the TNF family. A transmembrane activator and calcium-modulating and cyclophilin ligand interactor (TACI)-Ig fusion protein (which neutralizes both BAFF and a proliferation-inducing ligand (APRIL), another TNF family member) inhibited Hg-induced autoantibody or serum IgE production. These results are discussed in the context of the inhibitory effect of TACI-Ig on B cell maturation at the transitional stage.

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