The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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Published 7 February 2005. doi:10.1084/jem.20041557
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 201, Number 3, 325-331
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BRIEF DEFINITIVE REPORT

 Anthrax toxins suppress T lymphocyte activation by disrupting antigen receptor signaling

Silvia Rossi Paccani1, Fiorella Tonello3, Raffaella Ghittoni1,2, Mariarita Natale1, Lucia Muraro3, Mario Milco D'Elios4, Wei-Jen Tang5, Cesare Montecucco3, and Cosima T. Baldari1

1 Department of Evolutionary Biology, Policlinico Le Scotte, University of Siena, 53100 Siena, Italy
2 Department of Clinical Medicine and Immunological Sciences, Policlinico Le Scotte, University of Siena, 53100 Siena, Italy
3 Department of Biomedical Sciences, University of Padua, 35121 Padua, Italy
4 Department of Internal Medicine and Immunoallergology, University of Florence, 50134 Florence, Italy
5 Ben-May Institute for Cancer Research, University of Chicago, Chicago, IL 60637

CORRESPONDENCE Cosima T. Baldari: baldari{at}unisi.it

Anthrax is an infection caused by pathogenic strains of Bacillus anthracis, which secretes a three-component toxic complex consisting of protective antigen (PA), edema factor (EF), and lethal factor (LF). PA forms binary complexes with either LF or EF and mediates their entry into host cells. Although the initial phases of bacterial growth occur in the lymph node, the host fails to mount an effective immune response. Here, we show that LT and ET are potent suppressors of human T cell activation and proliferation triggered through the antigen receptor. Both LT and ET inhibit the mitogen-activated protein and stress kinase pathways, and both toxins inhibit activation of NFAT and AP-1, two transcription factors essential for cytokine gene expression. These data identify a novel strategy of immune evasion by B. anthracis, based on both effector subunits of the toxic complex, and targeted to a key cellular component of adaptive immunity.


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