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 Blood, 1 February 2008, Vol. 111, No. 3, pp. 1437-1447.
Prepublished online as a Blood First Edition Paper on November 8, 2007; DOI 10.1182/blood-2007-07-100404.

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IMMUNOBIOLOGY

A common pathway mediated through Toll-like receptors leads to T- and natural killer–cell immunosuppression

Ilan Vaknin1, Liora Blinder1, Lynn Wang1, Roi Gazit1, Elena Shapira1, Olga Genina2, Mark Pines2, Eli Pikarsky3, and Michal Baniyash1

1 Lautenberg Center for General and Tumor Immunology, Hebrew University Hadassah Medical School, Jerusalem; 2 Institute of Animal Science, Agricultural Research Organization, Volcani Center; and 3 Department of Pathology, Hebrew University Hadassah Medical School, Ein Kerem Campus, Kiryat Hadassah, Jerusalem, Israel

T- and natural killer (NK)–cell immunosuppression associated with {zeta}-chain down-regulation has been described in cancer, autoimmune, and infectious diseases. However, the precise stimuli leading to this bystander phenomenon in such different pathogen-dependent and sterile pathologies remained unresolved. Here, we demonstrate that Toll-like receptors (TLRs) play a major role in the induction of innate and adaptive immune system suppression; repetitive administration of single TLR 2, 3, 4, or 9 agonists, which do not exhibit any virulent or immune invasive properties, was sufficient to induce a bystander NK- and T-cell immunosuppression associated with {zeta}-chain down-regulation mediated by myeloid suppressor cells, as observed in the course of active pathologies. We identified a 35-amino acid (aa) region within the {zeta}-chain as being responsible for its degradation under TLR-mediated chronic inflammation. Furthermore, we provide evidence that {zeta}-chain levels could serve as a biomarker for chronic inflammation-dependent immunosuppression. Thus, although acute TLR-mediated activation could be beneficial in clearing pathogens or may serve as an immune adjuvant, such activation could be detrimental under sustained conditions.


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