Early cellular events in systemic autoimmunity driven by chromatin-reactive T cells

Cellular Immunology
A Kretz-Rommel, R L Rubin

Abstract

In vivo exposure of the thymus of normal mice to procainamide-hydroxylamine, a lupus-inducing drug, causes development of chromatin-reactive T cells. Autoantibodies subsequently appear, but their origin and significance are unknown. The current studies were undertaken to determine the specificities of B cells that respond to chromatin-reactive T cells at the initiation of this autoimmune process. Three days after adoptive transfer of 6 x 10(6) chromatin-reactive T cells, B cells with the capacity to secrete IgM anti-chromatin antibodies were detected in 1/10(6) splenocytes, and these became 10- to 50-fold more numerous if either the donor T cells or the recipient had defective Fas due to the lpr allele. Five days later these mice developed IgG anti-chromatin-secreting B cells at a precursor frequency of 3-6 x 10(-5). B cells with dDNA-binding activity isolated from mice primed in vivo to a complex of methylated pigeon cytochrome c and dDNA could stimulate naive, cytochrome c-reactive T cells in vitro, demonstrating that B cells can internalize dDNA-bound proteins through their dDNA immunoblobulin receptor and can functionally present a T cell epitope. However, no capacity of chromatin for binding anti-dDNA antibodies was detect...Continue Reading

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Citations

Jul 25, 2003·Toxicology and Applied Pharmacology·Michael J McCabeAllen J Rosenspire
Mar 16, 2005·Toxicology·Robert L Rubin
Jul 6, 2004·Clinics in Dermatology·Dimitar AntonovNikolai Tsankov
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May 30, 2003·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Eric BoilardMarc E Surette

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