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Metabolism shift T cells exhausten vs T cells senecence
- Thread starter Zara
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What happens when people get a virus with T cells and their metabolism?
In this book it is explained..especially in this part.
Source: the metabolic challenges of iimmune cells in health and disease.
T cells in this case cd8+ can get exhausted (eg hiv virus) or senescence ( in case of ebv or cmv). Interesting part is in the latter damage to mitochondria accures and lots of cytokines and chemokines are being produced. Hence inflammation reaction.
According to writer it starts with virus in tongsels..where T cells proliferate...
What is your opinion about this? Something like this accuring in me/cfs..?
Are there research data on this within me/cfs?
In this book it is explained..especially in this part.
Source: the metabolic challenges of iimmune cells in health and disease.
T cells in this case cd8+ can get exhausted (eg hiv virus) or senescence ( in case of ebv or cmv). Interesting part is in the latter damage to mitochondria accures and lots of cytokines and chemokines are being produced. Hence inflammation reaction.
According to writer it starts with virus in tongsels..where T cells proliferate...
What is your opinion about this? Something like this accuring in me/cfs..?
Are there research data on this within me/cfs?
pattismith
Senior Member
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full article here:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4174864/
"Although numerous infections are successfully cleared by the acute immune response, certain viral infections are not resolved and result in chronicity. The function of virus-specific T cells during chronic infections is often characterized by varying degrees of impairment, leading to defects in the ability of the host to eliminate the pathogen. Depending on the antigenic load generated by the infectious agent the impaired memory formation can result in T cells becoming either senescent or exhausted (9). Thus, immune senescence arises as a consequence of low-grade antigenic stimulation with the resulting inflammation determining the rate of senescence, as seen with CMV or EBV infection and not age per se (10, 11). The quantity of the lifelong antigenic load and the resulting inflammation determines the rate of immune senescence. Whereas a high-antigen load, caused by HIV, HCV, and HBV infection, leads to the formation of exhausted T cells (12)"
"Senescence manifests itself in T cells as the loss of the co-stimulatory molecule CD28 and the acquisition of innate markers such as killer-cell lectin-like receptor G1 (KLRG-1), while senescent T cells lose proliferative capacity they retain their cytotoxic activity and secretion of TNFα and IFNγ (17–19)."
"Senescent human CD8+ T cells isolated from healthy donors stimulated through the TCR have been shown to preferentially utilize glycolysis and also exhibit mitochondrial dysfunction and impaired mitochondrial biogenesis, which may explain their dependence on glycolysis for energy (17). The ability of a T cell to undergo mitochondrial biogenesis leads to an increased capacity of the cell to respond to metabolic stress, a characteristic termed spare respiratory capacity (2). It has been demonstrated that, unlike other memory subsets senescent CD8+ T cells have a substantially reduced spare respiratory capacity making them energetically unstable (17)."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4174864/
"Although numerous infections are successfully cleared by the acute immune response, certain viral infections are not resolved and result in chronicity. The function of virus-specific T cells during chronic infections is often characterized by varying degrees of impairment, leading to defects in the ability of the host to eliminate the pathogen. Depending on the antigenic load generated by the infectious agent the impaired memory formation can result in T cells becoming either senescent or exhausted (9). Thus, immune senescence arises as a consequence of low-grade antigenic stimulation with the resulting inflammation determining the rate of senescence, as seen with CMV or EBV infection and not age per se (10, 11). The quantity of the lifelong antigenic load and the resulting inflammation determines the rate of immune senescence. Whereas a high-antigen load, caused by HIV, HCV, and HBV infection, leads to the formation of exhausted T cells (12)"
"Senescence manifests itself in T cells as the loss of the co-stimulatory molecule CD28 and the acquisition of innate markers such as killer-cell lectin-like receptor G1 (KLRG-1), while senescent T cells lose proliferative capacity they retain their cytotoxic activity and secretion of TNFα and IFNγ (17–19)."
"Senescent human CD8+ T cells isolated from healthy donors stimulated through the TCR have been shown to preferentially utilize glycolysis and also exhibit mitochondrial dysfunction and impaired mitochondrial biogenesis, which may explain their dependence on glycolysis for energy (17). The ability of a T cell to undergo mitochondrial biogenesis leads to an increased capacity of the cell to respond to metabolic stress, a characteristic termed spare respiratory capacity (2). It has been demonstrated that, unlike other memory subsets senescent CD8+ T cells have a substantially reduced spare respiratory capacity making them energetically unstable (17)."
Last edited:
halcyon
Senior Member
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Yes this is occurring in ME. Several studies show increased PD-1 expression and decreased CD127 expression which are both exhaustion markers.
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Thanks guys ..
I found it also interesting to read the work of OMF is doing, one of the researcher of Standford..thesis: damage mitochondrial dna leading to difficulty or slowing of enzyme proccesing. When looking at picture of senescent Tcells it goes along with damaged mitochondria.
We are getting step by step closer to biomedical cause of ilness. Thanks to Ron Davis genius work and his gattering of a sublime team of experts from different medical fields.
I found it also interesting to read the work of OMF is doing, one of the researcher of Standford..thesis: damage mitochondrial dna leading to difficulty or slowing of enzyme proccesing. When looking at picture of senescent Tcells it goes along with damaged mitochondria.
We are getting step by step closer to biomedical cause of ilness. Thanks to Ron Davis genius work and his gattering of a sublime team of experts from different medical fields.