Trophoblast Apoptosis through TLR4 Heat Shock Protein 60 Induces Chlamydia
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High Sensitivity C–Reactive Protein and Im-munoglobulin G against Chlamydia Pneumo-niae and Chlamydial Heat Shock Protein-60 in Ischemic Heart Disease
Background: Inflammation and infectious agents such as Chlamydia pneumoniae have been associated with cardiovascular disease. Objective: To evaluate the serum high sensitivity C - reactive protein (hs-CRP) and antibodies against Chlamydia pneumoniae and Chlamydial heat shock protein-60 (Cp-HSP60) in patients with ischemic heart disease (IHD). Methods: 62 patients with IHD having either acute my...
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We recently reported that heat shock protein 60 (HSP60) via TLR4 signaling activates B cells and induces them to proliferate and secrete IL-10. We now report that HSP60 inhibits mouse B cell apoptosis, spontaneous or induced by dexamethasone or anti-IgM activation. Unlike HSP60 enhancement of B cell proliferation and IL-10 secretion, TLR4 signaling was not required for the inhibition of apoptos...
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Monocyte dysfunction by filarial antigens has been a major mechanism underlying immune evasion following hyporesponsiveness during patent lymphatic filariasis. Recent studies have initiated a paradigm shift to comprehend the immunological interactions of Wolbachia and its antigens in inflammation, apoptosis, lymphocyte anergy, etc. Here we showed that recombinant Wolbachia heat shock protein 60...
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Active inflammation and NF-kappaB activation contribute fundamentally to atherogenesis and plaque disruption. Accumulating evidence has implicated specific infectious agents including Chlamydia pneumoniae in the progression of atherogenesis. Chlamydial heat shock protein 60 (cHSP60) has been implicated in the induction of deleterious immune responses in human chlamydial infections and has been ...
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Infection, ischemia, trauma, and neoplasia elicit a similar inflammatory response in the CNS characterized by activation of microglia, the resident CNS monocyte. The molecular events leading from CNS injury to the activation of innate immunity is not well understood. We show here that the intracellular chaperone heat shock protein 60 (HSP60) serves as a signal of CNS injury by activating microg...
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