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#cytokines

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Giuseppe Michieli

Immunological #findings of West Caucasian #bat #virus in an accidental host biorxiv.org/cgi/content/short/

In #hamsters, #WCBV was highly pathogenic, determining 100% #lethality and mild #encephalitis. In comparison with Duvenhage virus (DUVV) and #RABV, we found that WCBV displayed an intermediate ability to promote cellular antiviral response, produce pro-inflammatory #cytokines, recruit and activate #lymphocytes in the hamsters central nervous system.

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Giuseppe Michieli

An ex vivo #human precision-cut #lung slice #platform provides insight into #SARS-CoV-2 #pathogenesis and #antiviral drug #efficacy, J Virol.: journals.asm.org/doi/full/10.1

We identified early induction of specific #cytokines, especially IP-10 and IL-8, as potential predictors for severe #COVID19, & uncovered a hitherto unrecognized phenomenon that while infectious virus disappears at late times of infection, viral #RNA persists and lung histopathology commences.

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Alan Lewis

A CAUSE OF INFLAMMATORY BOWEL DISEASE FOUND
Mastodon Post

BBC

Major cause of inflammatory bowel disease found
1 day ago

James Gallagher,Health and science correspondent

bbc.com/news/articles/c1wwdd6v

This is very serious business. Going on memory, my barber needed surgery because of long-term use of medication for Crohn's disease. He died of some complication from the surgery. He had the surgery, he seemed to be recovering well, and then, quite suddenly, he was gone.

:

#crohnsandcolitis #crohnsdisease #cytokines #franciscrickinstitute #inflammatoryboweldisease #inflammatorycolitis #jamesgallagher #jameslee #macrophages #medicalscience #medicalsciencenews #ruthwakeman #sciencenews #ulcerativecolitis #universitycollegelondon

:::

www.bbc.comMajor cause of inflammatory bowel disease foundScientists have found a weak spot in our DNA that is present in 95% of people with the disease.
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Monika Wolkers

Please find below our most recent pre-print. We studied the role of the RNA binding protein ZFP36L2 in effector T cells and found how it regulated the production of IFNgamma in late T cell responses and continuous activation with tumor cells (in vitro/in vivo). Happy reading!

biorxiv.org/content/10.1101/20

bioRxiv · Regulation of IFNγ production by ZFP36L2 in T cells is context-dependentCD8+ T cells kill target cells by releasing cytotoxic molecules and pro-inflammatory cytokines, such as TNF and IFNγ. The magnitude and duration of cytokine production is defined by post-transcriptional regulation, and a critical regulator herein are RNA-binding proteins (RBPs). Although the functional importance of RBPs in regulating cytokine production is established, the kinetics and mode of action through which RBPs control cytokine production is not well understood. Previously, we showed that the RBP ZFP36L2 blocks translation of pre-formed cytokine encoding mRNA in quiescent memory T cells. Here, we uncover that ZFP36L2 regulates cytokine production in a context-dependent manner. T cell-specific deletion of ZFP36L2 (CD4-cre) had no effect on T cell development, or on cytokine production during early time points (2-6h) of T cell activation. In contrast, ZFP36L2 specifically dampened the production of IFNγ during prolonged T cell activation (20-48h). ZFP36L2 deficiency also resulted in increased production of IFNγ production in tumour-infiltrating T cells that are chronically exposed to antigen. Mechanistically, ZFP36L2 regulates IFNγ production at late time points of activation by destabilizing Ifng mRNA in an AU-rich element-dependent manner. Together, our results reveal that ZFP36L2 employs different regulatory nodules in effector and memory T cells to regulate cytokine production. ### Competing Interest Statement The authors have declared no competing interest.
#Tcells#immunology#tumor
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Auscandoc

“By analyzing a longitudinal cohort of individuals infected with during the first wave of infections, Cai et al. found that subsequent against enhanced the frequency and functional qualities of -specific . Despite up-regulation of inhibitory receptors, spike-specific T cells produced more effector and cytotoxic molecules after ” mstdn.social/@erictopol/111546

Mastodon 🐘Eric Topol (@erictopol@mstdn.social)Vaccination after Covid does not lead to T cell exhaustion—it invigorates T cell functionality https://www.science.org/doi/10.1126/sciimmunol.adh0687
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halama_immuno

#innateimmunity in action: #immunotherapy against #breastcancer with TLR3 ligand and interferon alpha. Only six patients in this #trial , but biopsy analyses show improved #inmuneinfiltration with #TILs and is linked to clinical observations. #interferon #cytokines #immunology #macrophages @chfloudas
jitc.bmj.com/content/11/11/e00

Journal for ImmunoTherapy of Cancer · Systemic infusion of TLR3-ligand and IFN-α in patients with breast cancer reprograms local tumor microenvironments for selective CTL influxBackground Presence of cytotoxic T lymphocytes (CTL) in the tumor microenvironment (TME) predicts the effectiveness of cancer immunotherapies. The ability of toll-like receptor 3 (TLR3) ligands, interferons (IFNs) and COX2 inhibitors to synergistically induce CTL-attracting chemokines (but not regulatory T cell (Treg)-attractants) in the TME, but not in healthy tissues, observed in our preclinical studies, suggested that their systemic application can reprogram local TMEs. Methods Six evaluable patients (33–69 years) with metastatic triple-negative breast cancer received six doses of systemic chemokine-modulating (CKM) regimen composed of TLR3 ligand (rintatolimod; 200 mg; intravenous), IFN-α2b (20 MU/m2; intravenous) and COX2 inhibitor (celecoxib; 2×200 mg; oral) over 2 weeks. The predetermined primary endpoint was the intratumoral change in the expression of CTL marker, CD8α, in the post-CKM versus pre-CKM tumor biopsies. Patients received follow-up pembrolizumab (200 mg, intravenously, every 3 weeks), starting 3–8 days after completion of CKM. Results Post-CKM biopsies showed selectively increased CTL markers CD8α (average 10.2-fold, median 5.5-fold, p=0.034) and granzyme B (GZMB; 6.1-fold, median 5.8-fold, p=0.02), but not FOXP3 (Treg marker) relative to HPRT1 expression, resulting in the increases in average CD8α/FOXP3 ratio and GZMB/FOXP3 ratio. CKM increased intratumoral CTL-attractants CCL5 and CXCL10, but not Treg-attractants CCL22 or CXCL12. In contrast, CD8+ T cells and their CXCR3+ subset showed transient decreases in blood. One clinical response (breast tumor autoamputation) and three stable diseases were observed. The patient with clinical response remains disease free, with a follow-up of 46 months as of data cut-off. Conclusions Short-term systemic CKM selectively increases CTL numbers and CTL/Treg ratios in the TME, while transiently decreasing CTL numbers in the blood. Transient effects of CKM suggest that its simultaneous application with checkpoint blockade and other forms of immunotherapy may be needed for optimal outcomes. All data relevant to the study are included in the article or uploaded as supplementary information.
Public
PKPs Powerfromspace1

By @harryspoelstra COVID-19 promotes endothelial dysfunction and thrombogenicity: Role of pro-inflammatory #cytokines/SGLT2 pro-oxidant pathway

❗Finally we’re getting closer to understanding the underlying mechanisms, maybe even finding therapeutic possibilities, that of course need further research!

➡️"In #COVID19 patients, pro-inflammatory cytokines( f IL-1β, IL-6, TNF-α, MCP-1 and sICAM-1) induced a redox-sensitive up regulation of…
➡️Http://pubmed.ncbi.nlm.nih.gov

PubMedCOVID-19 promotes endothelial dysfunction and thrombogenicity: Role of pro-inflammatory cytokines/SGLT2 pro-oxidant pathway - PubMedIn COVID-19 patients, pro-inflammatory cytokines induced a redox-sensitive up-regulation of SGLT2 expression in ECs, which in turn promoted endothelial injury, senescence, platelet adhesion, aggregation, and thrombin generation. SGLT2 inhibition with empagliflozin, appeared as an attractive strategy …
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Auscandoc

people have lower levels of markers after infection news-medical.net/news/20230808 “The study published today in The Microbe found among individuals recently infected with , those who were fully vaccinated had lower concentrations of almost all markers ( and ) than those who were in the short-term and long-term after symptomatic SARS-CoV-2 infection.”

News-Medical.netVaccinated people have lower levels of inflammatory markers after COVID-19 infectionIn one of the largest studies of its kind, researchers provide answers to whether COVID-19 vaccinations reduce sickness and mortality following infection with SARS-CoV-2.
Replied in thread
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Arjan Boltjes

@gpollara @JExpMed Intriguing. In an earlier postdoc position I had a look at #DendriticCells, and especially the #cDC1 were abundant, but seemed to be just sitting in the inflammatory environment, doing little. One of the very abundant cytokines: #IL6

We also looked at the effect of that and other #cytokines, but mostly on #Tcells, among others due to the low abundance of cDC1 in HC blood to be able to do many in vitro experiments.

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Chuck Darwin

Healing from the hypothalamus –

To survive an infection, our body must recognize and respond to invading pathogens. This is the job of the immune system. When the first few immune cells encounter a pathogen, especially one that they haven’t seen before, they start releasing #cytokines like #interleukin-1 (IL-1).

These cytokines are the messengers of the immune system. They race through the body via the bloodstream, summoning immune troops to push back the invading pathogen.

When they reach the central nervous system, cytokines must cross the #blood-#brain #barrier to alert and recruit a brain response. The blood-brain barrier has only a handful of entry points, called #circumventricular #organs, where traffic can pass between the central nervous system and the bloodstream with relative ease.

One of these sits at the base of the #hypothalamus in a structure called the #Vascular #Organ of the #Lamina #Terminalis (VOLT for short). The #VOLT is filled with receptors that detect IL-1 and other cytokines.

That, along with its proximity to our #homeostat hypothalamus, means it’s positioned perfectly to sense an ongoing immune response and initiate our brain and body’s many defensive tactics.

After receiving signals from the VOLT, the hypothalamus creates many of the familiar experiences of sickness

pennneuroknow.com/2023/06/27/h

PennNeuroKnowHealing from the hypothalamusWhen we get hit with an infection, the reaction of a brain structure called the hypothalamus makes us feel sick – but its unpleasant responses are also important steps on the way to healing.
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