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Pellegrini, Marc; Calzascia, Thomas; Toe, Jesse G.; Preston, Simon P.; Lin, Amy E.; Elford, Alisha R.; Shahinian, Arda; Lang, Philipp A.; Lang, Karl S.; Morre, Michel; Assouline, Brigitte; Lahl, Katharina; Sparwasser, Tim; Tedder, Thomas F.; Paik, Ji-hye; DePinho, Ronald A.; Basta, Sameh; Ohashi, Pamela S.; Mak, Tak W.
Cell, 02/2011, Letnik: 144, Številka: 4Journal Article
Understanding the factors that impede immune responses to persistent viruses is essential in designing therapies for HIV infection. Mice infected with LCMV clone-13 have persistent high-level viremia and a dysfunctional immune response. Interleukin-7, a cytokine that is critical for immune development and homeostasis, was used here to promote immunity toward clone-13, enabling elucidation of the inhibitory pathways underlying impaired antiviral immune response. Mechanistically, IL-7 downregulated a critical repressor of cytokine signaling, Socs3, resulting in amplified cytokine production, increased T cell effector function and numbers, and viral clearance. IL-7 enhanced thymic output to expand the naive T cell pool, including T cells that were not LCMV specific. Additionally, IL-7 promoted production of cytoprotective IL-22 that abrogated liver pathology. The IL-7-mediated effects were dependent on endogenous IL-6. These attributes of IL-7 have profound implications for its use as a therapeutic in the treatment of chronic viral diseases. Display omitted ► Socs3 is upregulated in T cells during chronic active viral infection in mice ► Deletion of socs3 in T cells prevents immune failure and promotes viral clearance ► In vivo IL-7 therapy represses Socs3 in T cells and clears chronic infection ► IL-7 promotes IL-22 production to mitigate immunopathology in chronic infection
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Vir: Osebne bibliografije
in: SICRIS
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