66 research outputs found
Formation Mechanisms of Alloying Element Nitrides in Recrystallized and Deformed Ferritic Fe-Cr-Al Alloy
Continuous and discontinuous precipitation in Fe-1 at.%Cr-1 at.%Mo alloy upon nitriding; crystal structure and composition of ternary nitrides
Patellar resurfacing in posterior cruciate ligament retaining total knee arthroplasty (PATRES): design of a randomized controlled clinical trial
Nanoscale planar faulting in nanocrystalline Ni–W thin films: Grain growth, segregation, and residual stress
Low-Level Amplification of Oncogenes Correlates Inversely with Age for Patients with Nontypical Meningiomas
Preliminary investigations of a correlation between electron energy loss and morphometric analyses on ultrathin cryosections from normal and neoplastic gastric tissues
Temporal expression of the staphylococcal enterotoxin D gene under NaCl stress conditions
Mast cells elicit proinflammatory but not type I interferon responses upon activation of TLRs by bacteria
Balanced induction of proinflammatory and type I IFN responses upon activation of Toll-like receptors (TLRs) determines the outcome of microbial infections and the pathogenesis of autoimmune and other inflammatory diseases. Mast cells, key components of the innate immune system, are known for their debilitating role in allergy and autoimmunity. However, their role in antimicrobial host defenses is being acknowledged increasingly. How mast cells interact with microbes and the nature of responses triggered thereby is not well characterized. Here we show that in response to TLR activation by Gram-positive and -negative bacteria or their components, mast cells elicit proinflammatory but not type I IFN responses. We demonstrate that in mast cells, bound bacteria and TLR ligands remain trapped at the cell surface and do not undergo internalization, a prerequisite for type I IFN induction. Such cells, however, can elicit type I IFNs in response to vesicular stomatitis virus which accesses the cytosolic retinoic acid-inducible gene I receptor. Although important for antiviral immunity, a strong I IFN response is known to contribute to pathogenesis of several bacterial pathogens such as Listeria monocytogenes. Interestingly, we observed that the mast cell-dependent neutrophil mobilization upon L. monocytogenes infection is highly impaired by IFN-β. Thus, the fact that mast cells, although endowed with the capacity to elicit type I IFNs in response to viral infection, elicit only proinflammatory responses upon bacterial infection shows that mast cells, key effector cells of the innate immune system, are well adjusted for optimal antibacterial and antiviral responses
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