"Don't throw the baby out with the bath water." Regarding: 'No virus!' 'No GoF!' or 'All fake!' Not natural is not the same as 'not real'. Fraud and fakery may have been used, but something new exists
My friend is in hospital, UK, and it seems 50%+ of nurses are black Africans with their differing accents. UK has recruited from abroad for many years. Where my friend is, twice they stopped visitors for ten days when 2 different newly patients coughed, had elevated temperatures. Neither required any specialised treatment. All other patients required testing too, but not staff! Too many in NHS were positive having time off and causing staff shortages.
So much and Extinction event if prion involved, they are also transmitted via exosomes, and so many ways, no safe level and always fatal. They can’t be killed basically, and stick to everything and are in the soil for something like 15 years after clear up. They are taken up by plants, plants as vectors also.
My belief is that these labs are there to develop nasties which can be hidden in injections, disguised as healthcare, rather than as some super spreading infectious desease. The UK ran a cold clinic research centre for many years. Volunteers would book in for 2 weeks and many different attempts made to prove transmission. Not once could they do this. An aerosol disease that gets released then one person affects another. Gay men in US given Hep B prior. Africa given Smallpox prior. HIV and AIDS story.
AAAAARGH !!!!!! And as is typical, not ONE mention of how mRNA actually has destroyed people's hearts brains and organs, by making the T cells attack and destroy cells.
Doesn't matter how many times Dr bhakdi, Dr burkhart, John Campbell, Bret Weinstein, Marc GIRARDOT etc all repeatedly explained it.....everybody just can't comprehend the KILLER T CELLS ATTACKING.
It's utterly obvious, and proven in pathology , and yet yes, we are living in a sci fi horror movie where the whole planet collectively refuse to repeat the obvious answer.
Inflammasomes are the way macrophages and dendritic cells may kill, rather than the way killer T cells kill - but catechins from pomegranate peel can inhibit both the NET/inflammasome type and the MAIT CD8+ type. - based on the other searches.
**Do you want health solutions, or did you just want to vent some anger that the CoV activist doctors aren't doing enough? Cause I agree with that.
This one shows that NET/inflammasome is additional to what you seem to be talking about - but catechins help against either type.
Killer T Cells and Inflammasomes
Based on the provided search results, there is limited information directly addressing whether killer T cells (also known as cytotoxic T cells) use inflammasomes. However, we can infer some insights:
Inflammasomes are primarily associated with innate immune cells, such as macrophages and dendritic cells, where they play a crucial role in processing and releasing pro-inflammatory cytokines like IL-1β and IL-18. Killer T cells, being a type of adaptive immune cell, do not typically engage in inflammasome-mediated cytokine production.
The search results highlight the involvement of inflammasomes in T cells, but specifically in T helper cells and not in cytotoxic T cells (killer T cells). For example, a study mentioned in the PubMed snippet discusses the activation of inflammasomes in T helper cells, but not in cytotoxic T cells.
There is no direct evidence suggesting that killer T cells use inflammasomes for their cytotoxic functions, such as recognizing and killing virus-infected cells. Killer T cells primarily rely on their T-cell receptor (TCR) and co-stimulatory molecules to recognize and engage target cells, followed by the release of cytotoxins, such as perforin and granzymes, to induce apoptosis.
In conclusion, based on the available information, it appears that killer T cells do not use inflammasomes as part of their effector mechanisms. Instead, they employ their unique TCR-mediated recognition and cytotoxic pathways to eliminate infected cells.
Catechins, a class of polyphenolic compounds found in green tea, [*and pomegranate peel, sumac, and goji berries] have been shown to inhibit the activity of Mucosal-Associated Invariant T (MAIT) cells. Here, we summarize the key findings and mechanisms underlying this inhibition:
PTP1B inhibition: Catechins, particularly epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), have been demonstrated to inhibit the protein tyrosine phosphatase 1B (PTP1B) enzyme. PTP1B is overexpressed in breast cancer cells and contributes to tumor growth. MAIT cells, which are known to play a role in antitumor immunity, may be inhibited by catechins through PTP1B inhibition, potentially leading to reduced antitumor activity.
Modulation of macrophage phenotype: MAIT cells have been shown to regulate macrophage phenotype and function in liver fibrosis. Catechins may inhibit MAIT cells, leading to a shift in macrophage polarization from profibrogenic to restorative, thereby promoting liver fibrosis regression.
Immune regulatory networks: Catechins may also influence immune regulatory networks, potentially modulating the balance between pro-inflammatory and resolutive immune responses. This could contribute to the observed inhibition of MAIT cells and subsequent effects on liver fibrosis.
In summary, catechins have been found to inhibit MAIT T cells through multiple mechanisms, including PTP1B inhibition, modulation of macrophage phenotype, and immune regulatory network modulation. Further research is needed to fully elucidate the underlying mechanisms and potential therapeutic applications of catechin-mediated MAIT cell inhibition.
The catechins/tannins in pomegranate peel can inhibit inflammatory cytokine production by dendritic cells - https://www.mdpi.com/1422-0067/14/1/46/xml ; which would reduce the creation of killer T cells.
IL-1beta Boosts Killer T Cells
Dendritic cells (DCs) play a crucial role in initiating adaptive immune responses by processing and presenting antigens to T cells. IL-1β, a pro-inflammatory cytokine, is produced by DCs in response to various stimuli, including pathogen recognition and tissue damage. Research has shown that IL-1β produced by DCs has a direct impact on the development and activation of killer T cells (CD8+ T cells).
Mechanisms of IL-1β-Induced Killer T Cell Generation
DC licensing: IL-1β activates DCs to produce IL-12, a cytokine that licenses DCs to activate CD8+ T cells. This process involves the up-regulation of costimulatory molecules and the production of IL-12, which in turn activates CD8+ T cells.
T cell activation: IL-1β also directly activates CD8+ T cells by inducing the expression of activation markers and cytokines, such as IFN-γ and TNF-α. This activation enhances the cytotoxic activity of CD8+ T cells, enabling them to target infected cells or tumor cells more effectively.
Inflammasome activation: IL-1β can also activate the inflammasome, a multi-protein complex that processes pro-IL-1β and releases mature IL-1β. This amplifies the inflammatory response and enhances the activation of CD8+ T cells.
Consequences of IL-1β-Induced Killer T Cell Generation
Enhanced antitumor responses: IL-1β-induced killer T cell generation can enhance antitumor responses by promoting the activation and proliferation of CD8+ T cells, which can recognize and eliminate tumor cells.
Improved antimicrobial responses: IL-1β-induced killer T cell generation can also enhance antimicrobial responses by promoting the activation and proliferation of CD8+ T cells, which can recognize and eliminate infected cells.
Conclusion
In summary, IL-1β produced by dendritic cells plays a crucial role in enhancing the generation and activation of killer T cells (CD8+ T cells). This process involves DC licensing, T cell activation, and inflammasome activation, ultimately leading to enhanced antitumor and antimicrobial responses.
"This study shows that tumours induce the formation of NETs, which coat and thereby shield tumour cells against NK cell- and T cell-mediated cytotoxicity." https://www.nature.com/articles/s41577-020-0327-0
Brave AI
NET and Inflammasome in T Cells
Killer T cells, also known as cytotoxic T cells (CTLs), play a crucial role in eliminating infected or tumor cells. Recent studies have highlighted the involvement of neutrophil extracellular traps (NETs) and inflammasomes in the functioning of killer T cells.
NETs:
NETs are web-like structures formed by neutrophils in response to various stimuli, including pathogens and tumor cells.
Killer T cells can interact with NETs, which can modulate their effector functions.
NETs can provide a scaffold for killer T cells to adhere to and focus their cytotoxic activity on targeted cells.
Additionally, NETs can release antimicrobial peptides and proteins, which can enhance the antimicrobial activity of killer T cells.
Inflammasomes:
Inflammasomes are multi-protein complexes that activate caspase-1, leading to the processing and release of pro-inflammatory cytokines, such as IL-1β and IL-18.
Killer T cells can trigger inflammasome activation in antigen-presenting cells (APCs), such as dendritic cells and macrophages, through cognate interactions.
Activated inflammasomes can produce IL-1β, which can amplify the immune response and promote the recruitment of immune cells to the site of infection or tumor.
Inflammasome-independent IL-1β production has also been described in T cell-driven autoimmune diseases, highlighting the complexity of IL-1β regulation.
Interplay between NETs and Inflammasomes:
NETs can interact with inflammasomes, modulating their activity and influencing the production of IL-1β.
Inflammasome activation can also influence NET formation and release by neutrophils.
This interplay may be crucial for shaping the immune response and promoting effective elimination of pathogens or tumor cells.
If you want to know what happened.....here it is...... https://rumble.com/v5h388t-dr-j.-jay-couey.html?e9s=src_v1_ucp
My friend is in hospital, UK, and it seems 50%+ of nurses are black Africans with their differing accents. UK has recruited from abroad for many years. Where my friend is, twice they stopped visitors for ten days when 2 different newly patients coughed, had elevated temperatures. Neither required any specialised treatment. All other patients required testing too, but not staff! Too many in NHS were positive having time off and causing staff shortages.
Dr Philip Mc Millan..
https://t.me/PhilipMcMillan/2067 ➡️🟥➡️
What could go wrong?
So much and Extinction event if prion involved, they are also transmitted via exosomes, and so many ways, no safe level and always fatal. They can’t be killed basically, and stick to everything and are in the soil for something like 15 years after clear up. They are taken up by plants, plants as vectors also.
What’s happening in the gut of the injected also.
I was repeating the post punchline.
Yes, so much can go wrong. Man-made monstrosity unleashed on nature.
My belief is that these labs are there to develop nasties which can be hidden in injections, disguised as healthcare, rather than as some super spreading infectious desease. The UK ran a cold clinic research centre for many years. Volunteers would book in for 2 weeks and many different attempts made to prove transmission. Not once could they do this. An aerosol disease that gets released then one person affects another. Gay men in US given Hep B prior. Africa given Smallpox prior. HIV and AIDS story.
yes
CARLO BROGNA NEW STUDY
Could the Spike Protein Derived from mRNA Vaccines Negatively Impact Beneficial Bacteria in the Gut?
https://www.mdpi.com/2673-8112/4/9/97
Great paper, thanks for sharing it Solo!
Saw this had to give it to you
SHORT VIDEO
THE MIND BLOWING IMPACT OF LIGHT & SOUND ON THE MICROBIOME MARY RUDDICK
https://youtu.be/KEo_VXGhLOk
AAAAARGH !!!!!! And as is typical, not ONE mention of how mRNA actually has destroyed people's hearts brains and organs, by making the T cells attack and destroy cells.
Doesn't matter how many times Dr bhakdi, Dr burkhart, John Campbell, Bret Weinstein, Marc GIRARDOT etc all repeatedly explained it.....everybody just can't comprehend the KILLER T CELLS ATTACKING.
It's utterly obvious, and proven in pathology , and yet yes, we are living in a sci fi horror movie where the whole planet collectively refuse to repeat the obvious answer.
My May 13, 2020 post discusses pomegranate peel inhibition of NET which prevents killer Inflammasomes. https://open.substack.com/pub/denutrients/p/pomegranate-peel-catechins-inhibition-of-net-formation?r=os7nw&utm_campaign=post&utm_medium=web
You can't have understood anything I said
I said "nobody mentions KILLER T CELLS".
And then you didn't mention that.
Inflammasomes are the way macrophages and dendritic cells may kill, rather than the way killer T cells kill - but catechins from pomegranate peel can inhibit both the NET/inflammasome type and the MAIT CD8+ type. - based on the other searches.
**Do you want health solutions, or did you just want to vent some anger that the CoV activist doctors aren't doing enough? Cause I agree with that.
This one shows that NET/inflammasome is additional to what you seem to be talking about - but catechins help against either type.
Killer T Cells and Inflammasomes
Based on the provided search results, there is limited information directly addressing whether killer T cells (also known as cytotoxic T cells) use inflammasomes. However, we can infer some insights:
Inflammasomes are primarily associated with innate immune cells, such as macrophages and dendritic cells, where they play a crucial role in processing and releasing pro-inflammatory cytokines like IL-1β and IL-18. Killer T cells, being a type of adaptive immune cell, do not typically engage in inflammasome-mediated cytokine production.
The search results highlight the involvement of inflammasomes in T cells, but specifically in T helper cells and not in cytotoxic T cells (killer T cells). For example, a study mentioned in the PubMed snippet discusses the activation of inflammasomes in T helper cells, but not in cytotoxic T cells.
There is no direct evidence suggesting that killer T cells use inflammasomes for their cytotoxic functions, such as recognizing and killing virus-infected cells. Killer T cells primarily rely on their T-cell receptor (TCR) and co-stimulatory molecules to recognize and engage target cells, followed by the release of cytotoxins, such as perforin and granzymes, to induce apoptosis.
In conclusion, based on the available information, it appears that killer T cells do not use inflammasomes as part of their effector mechanisms. Instead, they employ their unique TCR-mediated recognition and cytotoxic pathways to eliminate infected cells.
https://search.brave.com/search?q=do+killer+T+cells+use+inflammasomes%3F&source=desktop&summary=1&summary_og=e03b01399b131402d0bd5a
Catechin Inhibits MAIT T cells
Catechins, a class of polyphenolic compounds found in green tea, [*and pomegranate peel, sumac, and goji berries] have been shown to inhibit the activity of Mucosal-Associated Invariant T (MAIT) cells. Here, we summarize the key findings and mechanisms underlying this inhibition:
PTP1B inhibition: Catechins, particularly epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), have been demonstrated to inhibit the protein tyrosine phosphatase 1B (PTP1B) enzyme. PTP1B is overexpressed in breast cancer cells and contributes to tumor growth. MAIT cells, which are known to play a role in antitumor immunity, may be inhibited by catechins through PTP1B inhibition, potentially leading to reduced antitumor activity.
Modulation of macrophage phenotype: MAIT cells have been shown to regulate macrophage phenotype and function in liver fibrosis. Catechins may inhibit MAIT cells, leading to a shift in macrophage polarization from profibrogenic to restorative, thereby promoting liver fibrosis regression.
Immune regulatory networks: Catechins may also influence immune regulatory networks, potentially modulating the balance between pro-inflammatory and resolutive immune responses. This could contribute to the observed inhibition of MAIT cells and subsequent effects on liver fibrosis.
In summary, catechins have been found to inhibit MAIT T cells through multiple mechanisms, including PTP1B inhibition, modulation of macrophage phenotype, and immune regulatory network modulation. Further research is needed to fully elucidate the underlying mechanisms and potential therapeutic applications of catechin-mediated MAIT cell inhibition.
https://search.brave.com/search?q=MAIT+T+cells+inhibition+by+catechins&source=desktop&summary=1&summary_og=746e048fe42a2ceccf2133
The catechins/tannins in pomegranate peel can inhibit inflammatory cytokine production by dendritic cells - https://www.mdpi.com/1422-0067/14/1/46/xml ; which would reduce the creation of killer T cells.
IL-1beta Boosts Killer T Cells
Dendritic cells (DCs) play a crucial role in initiating adaptive immune responses by processing and presenting antigens to T cells. IL-1β, a pro-inflammatory cytokine, is produced by DCs in response to various stimuli, including pathogen recognition and tissue damage. Research has shown that IL-1β produced by DCs has a direct impact on the development and activation of killer T cells (CD8+ T cells).
Mechanisms of IL-1β-Induced Killer T Cell Generation
DC licensing: IL-1β activates DCs to produce IL-12, a cytokine that licenses DCs to activate CD8+ T cells. This process involves the up-regulation of costimulatory molecules and the production of IL-12, which in turn activates CD8+ T cells.
T cell activation: IL-1β also directly activates CD8+ T cells by inducing the expression of activation markers and cytokines, such as IFN-γ and TNF-α. This activation enhances the cytotoxic activity of CD8+ T cells, enabling them to target infected cells or tumor cells more effectively.
Inflammasome activation: IL-1β can also activate the inflammasome, a multi-protein complex that processes pro-IL-1β and releases mature IL-1β. This amplifies the inflammatory response and enhances the activation of CD8+ T cells.
Consequences of IL-1β-Induced Killer T Cell Generation
Enhanced antitumor responses: IL-1β-induced killer T cell generation can enhance antitumor responses by promoting the activation and proliferation of CD8+ T cells, which can recognize and eliminate tumor cells.
Improved antimicrobial responses: IL-1β-induced killer T cell generation can also enhance antimicrobial responses by promoting the activation and proliferation of CD8+ T cells, which can recognize and eliminate infected cells.
Conclusion
In summary, IL-1β produced by dendritic cells plays a crucial role in enhancing the generation and activation of killer T cells (CD8+ T cells). This process involves DC licensing, T cell activation, and inflammasome activation, ultimately leading to enhanced antitumor and antimicrobial responses.
https://search.brave.com/search?q=dendritic+cells+IL-1beta+increase+killer+T+cells&source=desktop&summary=1&summary_og=99e3dad7b8945f15697180
I did make a document in 2020 about T cell balance, Th1/Th2 and the importance of reducing oxidative stress and increasing nutrients to support helpful T cell immunity and prevent autoimmunity. I didn't have the NET/inflammasome info in this document though. https://docs.google.com/document/d/1wXIZfyynEWAvTyOhvPX-iI7QJ5jyHbAj8t5yA0p-55Y/edit?usp=sharing
NET is involved with killer T cells.
"This study shows that tumours induce the formation of NETs, which coat and thereby shield tumour cells against NK cell- and T cell-mediated cytotoxicity." https://www.nature.com/articles/s41577-020-0327-0
Brave AI
NET and Inflammasome in T Cells
Killer T cells, also known as cytotoxic T cells (CTLs), play a crucial role in eliminating infected or tumor cells. Recent studies have highlighted the involvement of neutrophil extracellular traps (NETs) and inflammasomes in the functioning of killer T cells.
NETs:
NETs are web-like structures formed by neutrophils in response to various stimuli, including pathogens and tumor cells.
Killer T cells can interact with NETs, which can modulate their effector functions.
NETs can provide a scaffold for killer T cells to adhere to and focus their cytotoxic activity on targeted cells.
Additionally, NETs can release antimicrobial peptides and proteins, which can enhance the antimicrobial activity of killer T cells.
Inflammasomes:
Inflammasomes are multi-protein complexes that activate caspase-1, leading to the processing and release of pro-inflammatory cytokines, such as IL-1β and IL-18.
Killer T cells can trigger inflammasome activation in antigen-presenting cells (APCs), such as dendritic cells and macrophages, through cognate interactions.
Activated inflammasomes can produce IL-1β, which can amplify the immune response and promote the recruitment of immune cells to the site of infection or tumor.
Inflammasome-independent IL-1β production has also been described in T cell-driven autoimmune diseases, highlighting the complexity of IL-1β regulation.
Interplay between NETs and Inflammasomes:
NETs can interact with inflammasomes, modulating their activity and influencing the production of IL-1β.
Inflammasome activation can also influence NET formation and release by neutrophils.
This interplay may be crucial for shaping the immune response and promoting effective elimination of pathogens or tumor cells.
Conclusion:
The interplay between NETs and inflammasomes in killer T cells highlights the complexity of immune cell interactions and the multiple mechanisms by which they coordinate to eliminate pathogens or tumor cells. Further research is needed to fully understand the nuances of this interplay and its implications for immune-mediated diseases. https://search.brave.com/search?q=NET+and+inflammasome+role+in+killer+T+cells&source=desktop&summary=1&summary_og=a683675eb69589a50fd11c