The Journal of Experimental Medicine
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Published 7 September 2004. doi:10.1084/jem.20040358
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 200, Number 5, 637-646
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Molecular Characterization of Virus-induced Autoantibody Responses

Burkhard Ludewig1,2, Philippe Krebs1,2, Helen Metters1, Jutta Tatzel1, Özlem Türeci3, and Ugur Sahin3

1 Department of Pathology, Institute of Experimental Immunology, University Hospital Zürich, CH-8091 Zürich, Switzerland
2 Research Department, Kantonsspital St. Gallen, 9007 St. Gallen, Switzerland
3 Department of Internal Medicine, Johannes Gutenberg University Mainz, D-55131 Mainz, Germany

Address correspondence to Burkhard Ludewig, Research Department, Kantonsspital St. Gallen, Rotschacherstrasse 95, 9007 St. Gallen, Switzerland. Phone: 41-71-494-1090; Fax: 41-71-494-6321; email: burkhard.ludewig{at}kssg.ch

Here we present a comprehensive molecular mapping of virus-induced autoimmune B cell responses obtained by serological identification of antigens by recombinant expression cloning analysis. Immunoscreening of cDNA expression libraries of various organs (lung, liver, and spleen) using sera from mice infected with cytopathic (vaccinia virus [VV]) or noncytopathic (lymphocytic choriomeningitis virus [LCMV]) viruses revealed a broad specificity of the elicited autoantibody response. Interestingly, the majority of the identified autoantigens have been previously described as autoantigens in humans. We found that induction of virus-induced autoantibodies of the immunoglobulin G class largely depends on the CD40–CD40L-mediated interaction between T and B cells. Furthermore, antibody titers against a number of autoantigens were comparable to the concomitantly induced antiviral antibody response. Comparison of serum reactivity against a selected panel of autoantigens after infection with VV, LCMV, or vesicular stomatitis virus showed that the different virus infections triggered distinct autoantibody responses, suggesting that virus infections may leave specific "autoantibody fingerprints" in the infected host.

Key Words: autoantibodies • tumor immunity • virus-induced immunopathology • SEREX

B. Ludewig and P. Krebs contributed equally to this work.

Abbreviations used in this paper: COL13A1, procollagen XIII; GOLGB1, macrogolgin; LCMV, lymphocytic choriomeningitis virus; MYH6, myosin heavy chain {alpha}; ROCK, Rho-associated kinase; SEREX, serological identification of antigens by recombinant expression cloning; VSV, vesicular stomatitis virus; VV, vaccinia virus.


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