Calcium mobilizing treatment acts as a co-signal for TLR-mediated induction of Interleukin-12 (IL-12p70) secretion by murine bone marrow-derived dendritic cells

Huang, Emily; Showalter, Loral E; Xu, Shuwen; Czernliecki, Brian J.; Koski, Gary K.

doi:10.1016/j.cellimm.2017.01.010

Cited by 8 publications

(5 citation statements)

References 39 publications

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“…Whether other causes of calcium dyshomeostasis, including store‐operate calcium entry and second messenger‐operated calcium entry, are mechanistically active after CpG‐ODN exposure deserves further study. Previous reports have demonstrated that intracellular calcium affects CpG‐ODN‐induced gene expression, but whether this effect was mediated in part though cytosolic signalling was not investigated 93 . We believe that our findings are particularly relevant for understanding the role of TLR9‐mediated innate immune signalling and the pathogenesis of sterile inflammation.…”

Section: Discussionmentioning

confidence: 85%

CpG‐ODN‐mediated TLR9 innate immune signalling and calcium dyshomeostasis converge on the NFκB inhibitory protein IκBβ to drive IL1α and IL1β expression

et al. 2020

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Sterile inflammation contributes to many pathological states associated with mitochondrial injury. Mitochondrial injury disrupts calcium homeostasis and results in the release of CpG-rich mitochondrial DNA. The role of CpG-stimulated TLR9 innate immune signalling and sterile inflammation is well studied; however, how calcium dyshomeostasis affects this signalling is unknown. Therefore, we interrogated the relationship besween intracellular calcium and CpG-induced TLR9 signalling in murine macrophages. We found that CpG-ODN-induced NFjB-dependent IL1a and IL1b expression was significantly attenuated by both calcium chelation and calcineurin inhibition, a finding mediated by inhibition of degradation of the NFjB inhibitory protein IjBb. In contrast, calcium ionophore exposure increased CpG-induced IjBb degradation and IL1a and IL1b expression. These results demonstrate that through its effect on IjBb degradation, increased intracellular Ca 2+ drives a pro-inflammatory TLR9-mediated innate immune response. These results have implications for the study of innate immune signalling downstream of mitochondrial stress and injury.

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Section: Discussionmentioning

confidence: 85%

CpG‐ODN‐mediated TLR9 innate immune signalling and calcium dyshomeostasis converge on the NFκB inhibitory protein IκBβ to drive IL1α and IL1β expression

et al. 2020

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“…Electrical nociceptor activity induces in interacting DCs membrane depolarization and calcium influx, which may modulate myeloid cell functions ( 34 , 35 ). Indeed, calcium mobilization has been shown to increase IL-12 production by DCs upon TLR stimulation ( 36 ). Accordingly, coadministration of a calcium ionophore boosted the DC response to IMQ (fig.…”

Section: Nociceptor Activation Induces Membrane Depolarization In Int...mentioning

confidence: 99%

Multimodal control of dendritic cell functions by nociceptors

Hanč

González

Mazo

et al. 2023

Science

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It is known that interactions between nociceptors and dendritic cells (DCs) can modulate immune responses in barrier tissues. However, our understanding of the underlying communication frameworks remains rudimentary. Here, we show that nociceptors control DCs in three molecularly distinct ways. First, nociceptors release the calcitonin gene–related peptide that imparts a distinct transcriptional profile on steady-state DCs characterized by expression of pro–interleukin-1β and other genes implicated in DC sentinel functions. Second, nociceptor activation induces contact-dependent calcium fluxes and membrane depolarization in DCs and enhances their production of proinflammatory cytokines when stimulated. Finally, nociceptor-derived chemokine CCL2 contributes to the orchestration of DC-dependent local inflammation and the induction of adaptive responses against skin-acquired antigens. Thus, the combined actions of nociceptor-derived chemokines, neuropeptides, and electrical activity fine-tune DC responses in barrier tissues.

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“…These cascades of events govern immunostimulatory response while inhibits the Th2 adaptive immune responses. DNA nanostructures are the most promising carriers for immunizing various human diseases including (tuberculosis, hepatitis B, Alzheimer’s disease and malaria etc) [ 187 ]. King et al reported that DNA-based immunization is very successful in stimulating the humoral and cellular immune responses without triggering immunity against the vector.…”

Section: Potential Immuno-modulatory Effect Of Dna-based Nanostructuresmentioning

confidence: 99%

DNA Based and Stimuli-Responsive Smart Nanocarrier for Diagnosis and Treatment of Cancer: Applications and Challenges

Sabir

Zeeshan

Laraib

et al. 2021

Cancers

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The rapid development of multidrug co-delivery and nano-medicines has made spontaneous progress in tumor treatment and diagnosis. DNA is a unique biological molecule that can be tailored and molded into various nanostructures. The addition of ligands or stimuli-responsive elements enables DNA nanostructures to mediate highly targeted drug delivery to the cancer cells. Smart DNA nanostructures, owing to their various shapes, sizes, geometry, sequences, and characteristics, have various modes of cellular internalization and final disposition. On the other hand, functionalized DNA nanocarriers have specific receptor-mediated uptake, and most of these ligand anchored nanostructures able to escape lysosomal degradation. DNA-based and stimuli responsive nano-carrier systems are the latest advancement in cancer targeting. The data exploration from various studies demonstrated that the DNA nanostructure and stimuli responsive drug delivery systems are perfect tools to overcome the problems existing in the cancer treatment including toxicity and compromised drug efficacy. In this light, the review summarized the insights about various types of DNA nanostructures and stimuli responsive nanocarrier systems applications for diagnosis and treatment of cancer.

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Calcium mobilizing treatment acts as a co-signal for TLR-mediated induction of Interleukin-12 (IL-12p70) secretion by murine bone marrow-derived dendritic cells

Cited by 8 publications

References 39 publications

CpG‐ODN‐mediated TLR9 innate immune signalling and calcium dyshomeostasis converge on the NFκB inhibitory protein IκBβ to drive IL1α and IL1β expression

CpG‐ODN‐mediated TLR9 innate immune signalling and calcium dyshomeostasis converge on the NFκB inhibitory protein IκBβ to drive IL1α and IL1β expression

Multimodal control of dendritic cell functions by nociceptors

DNA Based and Stimuli-Responsive Smart Nanocarrier for Diagnosis and Treatment of Cancer: Applications and Challenges

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