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Modulation of granulocyte survival and programmed cell death by cytokines and bacterial products.
TLDR
Prolongation of survival may be important for the regulation of host resistance and inflammation, and may represent a crucial permissive step for certain cytokines and microbial products that activate gene expression and function in PMN.
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Toll-like Receptor 2 (TLR2) and TLR4 Differentially Activate Human Dendritic Cells*
TLDR
It is demonstrated that activation of dendritic cells by TLR2 or TLR4 agonists, although it led to comparable activation of NF-κB and mitogen-activated protein kinase (MAPK) family members, resulted in striking differences in cytokine and chemokine gene transcription, suggesting that TLR 2 andTLR4 signaling is not equivalent.
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Interleukin-1 type II receptor: a decoy target for IL-1 that is regulated by IL-4.
Interleukin-1 (IL-1) interacts with cells through two types of binding molecules, IL-1 type I receptor (IL-1R I) and IL-1R II. The function of IL-1R II is unknown. In studies using monoclonal…
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Cutting Edge: Inflammasome Activation by Alum and Alum’s Adjuvant Effect Are Mediated by NLRP31
TLDR
It is shown that alum-induced secretion of IL-1β, IL-18, and IL-33 is mediated by the NLR (nucleotide-binding domain leucine-rich repeat-containing) protein NLRP3 and its adaptor ASC, but not by NLRC4, suggesting that activation of theNLRP3-inflammasome may be a common mechanism of action of particulate adjuvants.
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Interleukin 1 signaling occurs exclusively via the type I receptor.
TLDR
It is concluded that a very small number of type I receptors is sufficient to mediate all of the actions of IL-1 which are examined here and that the function of the type II receptor may not be to transduce signals.
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Aluminum Hydroxide Adjuvants Activate Caspase-1 and Induce IL-1β and IL-18 Release1
TLDR
It is shown that Alum activates caspase-1 and induce secretion of mature IL-1β and IL-18, and a mechanism for the adjuvanticity of Alum is suggested.
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IL-10 Released by Concomitant TLR2 Stimulation Blocks the Induction of a Subset of Th1 Cytokines That Are Specifically Induced by TLR4 or TLR3 in Human Dendritic Cells1
TLDR
Each TLR appears to possess a distinctive ability to activate dendritic cells or PBMCs, suggesting that TLR-mediated responses cannot be simply cataloged as resembling either TLR2 (MyD88 dependent) or TLR4 ( myD88 independent) and that other signaling modalities may exist.
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Innate immune response to Francisella tularensis is mediated by TLR2 and caspase‐1 activation
Francisella tularensis, a gram‐negative, facultative, intracellular bacterium, is the etiologic agent of tularemia and a category A bioterrorism agent. Little is known about the mechanism of…
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Inflammasome-dependent Pyroptosis and IL-18 Protect against Burkholderia pseudomallei Lung Infection while IL-1β Is Deleterious
TLDR
It is shown that the Nod-like receptors (NLR) NLRP3 and NLRC4 differentially regulate pyroptosis and production of IL-1β and IL-18 and are critical for inflammasome-mediated resistance to melioidosis.
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Identification of Francisella tularensis Lipoproteins That Stimulate the Toll-like Receptor (TLR) 2/TLR1 Heterodimer*
TLDR
This study identifies for the first time specific Fran-cisella products capable of stimulating a proinflammatory response and the cellular receptors they trigger.
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