Immune Checkpoint
Aug 7, 2024 14:03:21 GMT
Post by Admin on Aug 7, 2024 14:03:21 GMT
When you think of Bartonella infection then it really operates like a cancer so you need to approach it like it’s cancer and you can do that with your immune system.
We can manipulate this to our advantage. Immunotherapy has arrived.
About the same time that Neil Spector said that the lyme microbes do the same thing that cancer does was when the Nobel Prize was awarded for cancer immunotherapy so it became clear that was where to focus, since nothing else was working very well.
medicine.duke.edu/news/spector-discusses-what-lyme-disease-has-common-cancer-recent-interview
"It's important to understand that because there may be ways to block it, and the answer may not be antibiotic-based."
Bcl-2, the B cell lymphoma protein is a protein that is part of a family of proteins involved in regulating cell death
www.ncbi.nlm.nih.gov/pmc/articles/PMC3255967/
“Intruders below the Radar: Molecular Pathogenesis of Bartonella spp.”
“Further experiments in the same study revealed a critical role of autocrine IL-8 signaling in the stimulation of endothelial cell proliferation and angiogenic phenotypes in response to B. henselae infection. The mitogenic stimulus was accompanied by a potent antiapoptotic effect via a strong increase in the ratio of Bcl-2 to Bax”
www.ncbi.nlm.nih.gov/pmc/articles/PMC123703/
“Bartonella-associated endothelial proliferation depends on inhibition of apoptosis”
“In vivo, Bartonella causes angioproliferative diseases involving the formation of numerous immature vessels (6, 25–27). The results of our study raise the obvious question of whether inhibition of apoptosis also might lead to endothelial proliferation and, hence, angioproliferation in vivo. Indeed, emerging evidence shows that cells of the neovasculature are critically dependent on antiapoptotic signals for their survival (28–30). Experimentally suppressing apoptosis by increasing Bcl-2 levels promotes angiogenesis in tumors (31), whereas withdrawal of antiapoptotic survival signals leads to regression of vessels”
www.ncbi.nlm.nih.gov/pmc/articles/PMC9950219/
“BCL-2 protein family: attractive targets for cancer therapy”
www.ncbi.nlm.nih.gov/pmc/articles/PMC5920861/
"Solamargine derived from Solanum nigrum induces apoptosis of human cholangiocarcinoma QBC939 cells"
"In addition, western blot analysis demonstrated that solamargine inhibited the protein expression of Bcl-2"
Bcl-2 is a main checkpoint that bartonella uses and fucoidan makes the checkpoint inhibitor work better;
bartonella.freeforums.net/thread/136/bcl-2
You need to treat Bartonella infection like it’s cancer.
bartonella.freeforums.net/thread/125/angiogenesis
~d
We can manipulate this to our advantage. Immunotherapy has arrived.
About the same time that Neil Spector said that the lyme microbes do the same thing that cancer does was when the Nobel Prize was awarded for cancer immunotherapy so it became clear that was where to focus, since nothing else was working very well.
medicine.duke.edu/news/spector-discusses-what-lyme-disease-has-common-cancer-recent-interview
"It's important to understand that because there may be ways to block it, and the answer may not be antibiotic-based."
Bcl-2, the B cell lymphoma protein is a protein that is part of a family of proteins involved in regulating cell death
www.ncbi.nlm.nih.gov/pmc/articles/PMC3255967/
“Intruders below the Radar: Molecular Pathogenesis of Bartonella spp.”
“Further experiments in the same study revealed a critical role of autocrine IL-8 signaling in the stimulation of endothelial cell proliferation and angiogenic phenotypes in response to B. henselae infection. The mitogenic stimulus was accompanied by a potent antiapoptotic effect via a strong increase in the ratio of Bcl-2 to Bax”
www.ncbi.nlm.nih.gov/pmc/articles/PMC123703/
“Bartonella-associated endothelial proliferation depends on inhibition of apoptosis”
“In vivo, Bartonella causes angioproliferative diseases involving the formation of numerous immature vessels (6, 25–27). The results of our study raise the obvious question of whether inhibition of apoptosis also might lead to endothelial proliferation and, hence, angioproliferation in vivo. Indeed, emerging evidence shows that cells of the neovasculature are critically dependent on antiapoptotic signals for their survival (28–30). Experimentally suppressing apoptosis by increasing Bcl-2 levels promotes angiogenesis in tumors (31), whereas withdrawal of antiapoptotic survival signals leads to regression of vessels”
www.ncbi.nlm.nih.gov/pmc/articles/PMC9950219/
“BCL-2 protein family: attractive targets for cancer therapy”
www.ncbi.nlm.nih.gov/pmc/articles/PMC5920861/
"Solamargine derived from Solanum nigrum induces apoptosis of human cholangiocarcinoma QBC939 cells"
"In addition, western blot analysis demonstrated that solamargine inhibited the protein expression of Bcl-2"
Bcl-2 is a main checkpoint that bartonella uses and fucoidan makes the checkpoint inhibitor work better;
bartonella.freeforums.net/thread/136/bcl-2
You need to treat Bartonella infection like it’s cancer.
bartonella.freeforums.net/thread/125/angiogenesis
~d