Differential regulation of proinflammatory mediators following LPS- and ATP-induced activation of monocytes from patients with antiphospholipid syndrome.
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Cites background from "Differential regulation of proinfla..."
...It is a widely accepted view that pathogenesis of many autoimmune diseases is largely driven by inappropriate or inadequate immune responses toward bacterial agents (50, 51)....
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Cites background from "Differential regulation of proinfla..."
...Monocytes have been recognized as key cells for the pathogenesis of APS [11] and previous “in vitro” and clinical studies have demonstrated an increased activation of monocytes in patients with APS [27,28]....
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...For the pathogenesis of thrombotic APS, the immune-complex formed by aCL or aβ2GP1 and their antigens, in particular LDL oxidized, would activatemonocytes to express tissue factor, to secrete inflammatory cytokines [11,27] and possibly contribute to the formation of atherosclerotic plaques on the vascular wall [30]....
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References
733 citations
"Differential regulation of proinfla..." refers background in this paper
...InappropriateTh17 activation was shown to play a crucial role in the induction/maintenance of multiple types of diseases, including autoimmune tissue injury [38]....
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"Differential regulation of proinfla..." refers background in this paper
...In particular, the P2X7 receptor has attracted considerable interest since its activation triggers maturation and release of proinflammatory IL-1β in monocytes and macrophages [46]....
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336 citations
"Differential regulation of proinfla..." refers background in this paper
...Currently, mechanisms by which microbial agents trigger autoimmune reaction include induction of pathogenic autoantibody production as a result of molecular mimicry and cross reactivity [29] and polyclonal activation of distinct T cell subclasses [27]....
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...Autoimmune diseases have a multifactorial etiology depending on both genetic and environmental factors [27]....
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309 citations
"Differential regulation of proinfla..." refers background in this paper
...Several mechanisms have been proposed for how autoantibodies cause the disease, including interaction with cell surface receptors, such as TLR/IL-1 receptor family members [3], annexin A2 [4], and activation of the complement complex in vessels [5]....
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