Journal of Clinical and Cellular Immunology
Open Access
ISSN: 2155-9899
ISSN: 2155-9899
Luis I Terrazas, Sandy Reyes, Yolanda Hernández and Yadira Ledesma-Soto
Posters-Accepted Abstracts: J Clin Cell Immunol
It has been largely appreciated that helminth infections modulate the immune response of their hosts, but mechanisms involved in such modulation are not entirely known. Macrophages and dendritic cells appear to be consistently affected during these types of infections and are common target cells for helminth-derived molecules. Here we found that macrophages obtained from chronically Taenia crassiceps-infected mice, displayed an impaired response to TNF-α, IFN-γ but not to IL-4 neither IL-6, measured through the phosphorylation of NF-kB, STAT1, STAT6 and STAT3, respectively. At the same time, such macrophages expressed high levels of SOCS3. Interestingly, exposure of naïve murine macrophages to excreted/secreted products from T. crassiceps (TcES) similarly interfered with the signaling of these cytokines. Moreover, macrophages exposed to TcES expressed high levels of SOCS3 as well as phosphatase SHP1. Strikingly, inhibition of phosphatases abrogated the impaired IFN-γ-signaling induced by TcES. Together these data demonstrate a new mechanism by which helminth derived products target intracellular pathways to block macrophage response to inflammatory cytokines.