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Modulation of granulocyte survival and programmed cell death by cytokines and bacterial products.
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.
Toll-like Receptor 2 (TLR2) and TLR4 Differentially Activate Human Dendritic Cells*
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.
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…
Cutting Edge: Inflammasome Activation by Alum and Alum’s Adjuvant Effect Are Mediated by NLRP31
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.
Interleukin 1 signaling occurs exclusively via the type I receptor.
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.
Aluminum Hydroxide Adjuvants Activate Caspase-1 and Induce IL-1β and IL-18 Release1
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.
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
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.
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…
Inflammasome-dependent Pyroptosis and IL-18 Protect against Burkholderia pseudomallei Lung Infection while IL-1β Is Deleterious
- I. Ceballos-Olvera, M. Sahoo, Mark A. Miller, Laura Tabuenca del Barrio, F. Re
- Biology, MedicinePLoS pathogens
- 1 December 2011
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.
Identification of Francisella tularensis Lipoproteins That Stimulate the Toll-like Receptor (TLR) 2/TLR1 Heterodimer*
This study identifies for the first time specific Fran-cisella products capable of stimulating a proinflammatory response and the cellular receptors they trigger.