#interferons

[wheelie-sick]

*my class lecture is about interferons and mast cells*

internally: I KNOW ABOUT THOSE MINE ARE BROKEN

I get so excited when I know stuff in the lecture like yeah I know what interferons are. I don't have any anymore! they're gone! goodbye and good riddance!

[sodrippy]

prednisone is a beautiful name for a baby girl

[willowreader]

This analysis made it clear that the difference between those who were improving and those who were not was in the immune system’s interferon-led response to the virus. Interferons are proteins that act like the body’s alarm system against viruses and other harmful invaders. When a virus infects a cell, the cell sends out interferons to warn nearby cells. These nearby cells then prepare to defend themselves, making it harder for the virus to spread. All of these responses produce specific biological signatures that have been determined in various experiments and exist in databases.

This article explains how interferons in our cells can help some people recover from brain fog ir cognitive impairment in Long Covid.

[bpod-bpod]

Reining-in Flaviviruses

Flaviviruses have existed for thousands of years and still hit the headlines, most recently with Zika virus. They can fatally infect the human brain. Your body defends against them by making the protein interferon type I (IFN-I). How IFN-I affects the ability of flaviviruses to infect different cells (tropism), which determines the infection's spread, isn't clear. Researchers investigate by infecting the brains of normal mice and mice genetically altered so they're unresponsive to IFN-I, with the flavivirus, Langat virus. Combining optical projection tomography (OPT) with MRI revealed virus distribution in the brain (pictured). In normal mice (two views left), the virus only infected grey matter in sensory brain areas. In mutants (right), it spread further, infecting white matter. The team revealed the spread into white matter-targeted cells called microglia. Normal mice brains had more IFN-I activity, which protected microglia, uncovering IFN-I's role in viral tropism.

Written by Lux Fatimathas

Image from work by Nunya Chotiwan, Ebba Rosendal and Stefanie M. A. Willekens, and colleagues

Department of Clinical Microbiology, Umeå University, Umeå, Sweden

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Nature Communications, April 2023

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[medicomunicare]

I farmaci modificanti della malattia (DMARDs): un cardine essenziale per trattare le malattie autoimmuni

I farmaci modificanti il decorso della malattia (Disease-Modifying Antirheumatic Drugs; DMARDs) sono una classe di farmaci utilizzati principalmente nelle malattie autoimmuni e reumatologiche per modificare il decorso della malattia e rallentare la progressione del danno tissutale, migliorando la qualità della vita e riducendo i sintomi. I DMARDs comprendono farmaci convenzionali sintetici,…

[colinwilson11]

The cGAS-STING Pathway: A Key Immune Surveillance Mechanism

The innate immune system provides the first line of defense against invading pathogens like viruses and bacteria. One of its key mechanisms for detecting microbial infections is the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway. This cellular surveillance pathway plays a critical role in detecting foreign DNA from invading microbes and mounting appropriate immune responses.

How It Works

When microbial DNA enters the cytosol of host cells, it is recognized by the cGAS enzyme. cGAS has the unique ability to bind to DNA and produce the second messenger cyclic GAMP (cGAMP) from ATP and GTP. cGAMP then acts as a ligand to bind and activate the endoplasmic reticulum-associated adaptor protein called STING.

Activation of STING leads to its association with tumor necrosis factor receptor-associated factor 3 and 6 (TRAF3/6). This triggers a downstream signaling cascade involving the protein kinases TANK-binding kinase 1 (TBK1) and interferon regulatory factor 3 (IRF3).

Phosphorylation of IRF3 by TBK1 causes IRF3 dimerization and translocation into the host cell nucleus. There, IRF3 induces the expression of Type I interferons (IFN-α and IFN-β) and other proinflammatory cytokines that signal the presence of invading pathogens to other cells and recruit additional immune defenses.

Role In Antiviral Defense

The cGAS-STING Pathway plays a critical role in the host defense against various DNA viruses like herpes simplex virus 1, cytomegalovirus, Epstein-Barr virus, vaccinia virus and HIV. Upon viral DNA entry in the cytosol, cGAS binds and activates STING to induce Type I IFN production. This initiates an antiviral state in infected cells and neighboring uninfected cells to limit viral replication and spread. Mice lacking cGAS or STING exhibit impaired IFN responses and increased susceptibility to infection by these DNA viruses.

Protecting Against Cancer

Aside from fighting infections, the cGAS-STING Pathway also acts as a tumor suppressor mechanism by detecting aberrant genomic DNA in cancer cells. Many cancer cells have disruptions like broken DNA strands that could lead to cell death if sensed by the immune system. However, cancer cells often develop ways to evade this cGAS-STING surveillance.

Studies have shown that loss of or reduced expression and activity of cGAS or STING promotes tumorigenesis in various cancer types like colon cancer and prostate cancer. At the same time, therapeutically activating the cGAS-STING Pathway seems to stimulate antitumor immunity and enhance the effectiveness of cancer immunotherapies in mouse models. This highlights the pathway's potential for developing new immunotherapeutic strategies against cancer.

Role In Autoimmune Disease

While the cGAS-STING Pathway protects against infections and tumors, its overactivation can also lead to inflammatory and autoimmune conditions. Defects that cause constitutive STING signaling have been linked to autoinflammatory diseases. Genetic mutations that make STING hyperactive and uncontrollable result in a group of rare hereditary inflammatory syndromes known as STING-associated vasculopathies with onset in infancy (SAVI). Patients with SAVI exhibit symptoms resembling systemic lupus erythematosus due to excess Type I IFN production.

Meanwhile, environmental and endogenous cytosolic DNA from dying cells have been shown to aberrantly trigger the cGAS-STING Pathway and IFN responses during conditions like systemic lupus erythematosus or Aicardi-Goutières syndrome. Figuring out ways to modulate cGAS-STING activation or signaling may yield new therapeutic approaches for these diseases.

Pharmaceutical Applications

Given its crucial contribution to antiviral immunity and cancer immunosurveillance, the cGAS-STING Pathway represents an attractive target for pharmaceutical intervention. Small molecule drugs that activate cGAS or STING are being developed as potential antiviral and anticancer agents. STING agonists administered alone or in combination with checkpoint inhibition immunotherapy show promise in treating solid tumors in clinical trials.

Moreover, cGAS or STING inhibitors may offer new ways to treat autoinflammatory conditions caused by overactive cGAS-STING signaling. Researchers continue working to refine drugs that can selectively modulate different points along the pathway for optimal therapeutic benefit while avoiding side effects. As understanding of this defense mechanism deepens, more opportunities may arise to harness it against an array of diseases with immunological underpinnings.

The cGAS-STING Pathway serves as a critical surveillance system helping our innate immune defenses detect cytosolic DNA. Its ability to sense microbial as well as aberrant self-DNA makes it an important regulator of antiviral immunity, tumor suppression, and inflammatory balance. Ongoing investigations into modulating cGAS-STING activation hold promise for developing new immunotherapies targeting infections, cancer, and autoimmune disorders.

Get more insights on this topic:   https://www.ukwebwire.com/role-of-cgas-sting-pathway-in-detecting-cytosolic-dna/

Author Bio:

Alice Mutum is a seasoned senior content editor at Coherent  Insights, leveraging extensive expertise gained from her previous role as a content writer. With seven years in content development, Alice masterfully employs SEO best practices and cutting-edge digital ing strategies to craft high-ranking, impactful content. As an editor, she meticulously ensures flawless grammar and punctuation, precise data accuracy, and perfect alignment with audience needs in every research report. Alice's dedication to excellence and her strategic approach to content make her an invaluable asset in the world of  insights. (LinkedIn: www.linkedin.com/in/alice-mutum-3b247b137 )

*Note: 1. Source: Coherent  Insights, Public sources, Desk research 2. We have leveraged AI tools to mine information and compile it

[anmapvnn]

GLUKAFERON

Interferon

[organichealthsolutions]

How Do Supplements Lead to Anti-Aging?

Millions of men and women aim to slow down the signs of aging while achieving a more youthful, radiant look. While skincare products, particularly serums, can help you achieve that, many seek approaches that lead to improvements from the inside out.

Anti-aging supplements are becoming more popular than ever. These products promote results from a cellular level. But how do they work?

What are Anti-Aging Supplements?

Supplements that fall under the anti-aging category aim to slow down the signs of aging. Depending on their formulation, that could mean promoting more refreshed and youthful skin. However, many products can also translate to better health and vitality.

Whatever the case, they work from the inside out. While traditional anti-aging skincare products are topical, these supplements are oral. That means you consume them much like your daily multivitamin!

Anti-aging supplements can come in gummy, tablet, capsule or liquid form. Whether you get a selenium supplement that protects from sun exposure or an anti aging polyphenols supplement formulated to provide multiple benefits, the main difference is that you consume these supplements.

How Do Anti-Aging Supplements Work?

The magic comes from the ingredients. These products contain ingredients that improve your skin and slow down the signs of aging at a cellular level. While your diet and supplement regime greatly keep you healthy, these supplements focus on keeping your cells young to deliver anti-aging benefits and more vitality.

Anti aging polyphenols supplement products are some of the best because they contain powerful plant compounds. Polyphenols are compounds that keep plants safe from ultraviolet radiation and oxidative stress. Studies are showing that humans can reap the same benefits and more.

Researchers found that polyphenols are effective in providing many anti-aging properties. They're potent antioxidants that neutralize damaging free radicals while protecting cells from oxidative stress. That protects your DNA from damage.

Polyphenols are also robust anti-inflammatories that tame inflammatory responses. Research suggests they also have anticancer properties.

Overall, polyphenols are the ingredient to success in the fight against aging. While aging is natural, supplements can make a difference by reducing the effects aging has on your appearance and vitality.

Read a similar article about supplement for artery protection here at this page.

[academiavet]

Efeitos terapêuticos do interferon ômega felino (rFeIFN-ω) na evolução clínica de gatos naturalmente infectados com imunodeficiência felina (FIV) e vírus da leucemia felina (FeLV)

O rFeIFN-ω mostrou-se útil na melhora da sintomatologia clínica e no controle de infecções virais secundárias em gatos FIV+, FeLV+ e FIV/FeLV+.

Referência:

Cravo, J.A.P. (2011). Efeito do tratamento por interferão ómega de origem felina (rFeIFN-Ω) na evolução clínica de gatos naturalmente infectados com os vírus da imunodeficiência (FIV) e leucemia felinas (FeLV) e na excreção de vírus respiratórios concomitantes. Dissertação de Mestrado. Universidade Técnica de Lisboa, Faculdade de Medicina Veterinária, Lisboa.

[pwrn51]

How one Woman became a Trailblazer for Cancer

  Betsy’s guest is Judith L. Pearson, an award-winning author, and writer, who’s here to discuss her latest book, “CRUSADE TO HEAL AMERICA: The Remarkable Life of Mary Lasker.” In our conversation, Judy highlights the incredible story of Mary Lasker, a health activist and philanthropist, known for her passionate stance, “I am opposed to heart disease and cancer the way one is opposed to…

[deinheilpraktiker]

Wie moduliert das ISG15/ISGylierungssystem die Infektion mit dem Vaccinia-Virus?

In einer aktuellen Studie, die im veröffentlicht wurde bioRxiv* Server zeigten Forscher, wie das Interferon-stimulierte Gen 15 (ISG15) an der Verbreitung des Vaccinia-Virus (VACV) beteiligt ist. Studie: ISG15 ist für die Verbreitung extrazellulärer Virionen des Vaccinia-Virus erforderlich. Bildnachweis: Kateryna Kon/Shutterstock Bei diesem Nachrichtenartikel handelte es sich um eine Rezension…

[ricisidro]

View this post on Instagram

A post shared by Jun Isidro (@rcisidro)

Our first line of defense vs #SARSCoV2 are interferons, our innate immunity, a complex system not yet exploited for prevention and therapy. A great new review/perspective here @ImmunityCP | via Eric Topol @EricTopol

Innate immunity and interferon in SARS-CoV-2 infection outcome, published in Immunity on 06.18.23

[pepikhipik]

Riziko sebevraždy u hepatitidy C a během léčby interferonem alfa

Buňky naší imunity úzce spolupracují s mozkem, ovlivňují náladu, chuť k jídlu, ale i deprese. Inferferon-alfa je protivirová molekula produkovaná našimi imunitními buňkami. Když se před lety pokoušeli poprvé využít interferon-alfa (produkt imunitních buněk) k léčbě chronické žloutenky typu C netušili, že mnoho pacientů po zahájení léčby spáchá sebevraždu. Ukázalo se, že tento cytokin (v našem těle velmi citlivě regulovaný imunitními buňkami), vyvolává u některých lidí při vyšších koncentracích sebevražedné myšlenky.

Odkaz na relevantní studie:

Suicide risk in hepatitis C and during interferon-alpha therapy: a review and clinical update

[cilginfizikcilervbi]

Down Sendromumlular Neden Daha Az Hasta Olur Ama Ağır Geçirir?

Down Sendromumlular Neden Daha Az Hasta Olur Ama Ağır Geçirir? Down sendromu, trizomi 21 ya da mongolizm; genetik düzensizlik sonucu insanın 21. kromozom çiftinde fazladan bir kromozom bulunması durumu ve bunun sonucu olarak ortaya çıkan genetik bir bozukluktur. Down Sendromumlular Neden Daha Az Hasta Olur Ama Ağır Geçirir? Down sendromuna (DS) tipik olarak 21. kromozomun üçlenmesi neden olur.…

[bpod-bpod]

Stop Interferon

When we’re ill, the body’s immune system prepares a cocktail of chemicals – some to rally our defences, others to warn our cells. But we may be warning something else too. Researchers looking at mice playing host to Ixodes scapularis ticks (like this one, given artificial fluorescence), found the ticks respond to a specific chemical found in their blood meal. Unusually for a different species, the ticks have a receptor – a protein that 'catches' another chemical – that fits a mammalian chemical called interferon gamma like a glove. The receptor, Dome-1, then triggers a series of changes inside the tick. Researchers find that these cross-species signals help the tick to adapt, grow and feed, but also bolster its immunity, protecting the parasite. While the team investigate such communication across an evolutionary divide, their studies may inspire drugs designed to guide or block these chemical messages.

Written by John Ankers

Image from work by Vipin S. Rana and colleagues, Utpal Pal Lab

Department of Veterinary Medicine, University of Maryland, College Park, MD, USA

Image copyright held by the original authors

Research published in Science, January 2023

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[medicomunicare]

I progressi biotecnologici sulle staminali: dal risveglio delle dormienti alla possibilità di produrle in metà tempo

Nel cervello adulto dei mammiferi, la maggior parte delle cellule staminali neurali, che hanno origine dal sistema nervoso e possono trasformarsi in vari tipi di cellule cerebrali, rimangono dormienti finché non ricevono segnali specifici che le attivano. Una volta risvegliate, producono nuovi neuroni, aiutando la riparazione e la crescita del cervello. I difetti nell’attivazione delle cellule…