§ɦṛɛɗɗịɛ ßịⱺ𝔩ⱺɠịᵴŧ

“I would rather have questions that can’t be answered than answers that can’t be questioned.” - Rich Feynman

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Joined 2 years ago
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Cake day: March 19th, 2022

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  • Well, in digging into some research papers, I found “mast cell activation can be caused by both IgE-mediated and non–IgE-mediated triggers”.

    This is because there can be a mast cell mutation (KIT) which then doesn’t require IgE for activation. You have MMAS and not Mastocytosis, right? The mutation seems to be associated with Mastocytosis based on my understanding from the paper.

    Since mast cells aren’t privileged, they’re restricted from entering sites like the brain and spinal cord. So, if they’re in the spinal cord, you almost certainly have bigger problems than mast cell activation I’d think, as the barrier isn’t doing it’s job.

    In case you’re interested, here’s the paper on mast cell disorders: https://www.jacionline.org/article/S0091-6749(17)31025-4/fulltext

    Here’s one on the brain and spinal cord: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3481533/

    The BIGGEST issue with our understanding of the immune system today is that ALL testing is done on mice. The human body on a chip technology along with the digitization of the immune system together will be a monumental step. Thankfully, it’s literally something we’ll have in the near future. Once that’s available, we’ll have human specific data plus an onslaught of constant information, which we need to help folks with all of the immune system disorders. I’m an autoimmune patient and losing my friends and family to this uncertainty has led me into the field to try and help improve our understanding. There’s legit more we don’t know than we do know about the human immune system right now.




  • While there’s no free floating IgE in your system, to degranulate mast cells need IgE bound to their surface. Thats the activation aspect. Since you need mast cells, it’s not exactly something you can turn off. Glad you know the triggers at least, gives you the opportunity to make moves accordingly!

    Here’s a great image of degranulation:

    You need two IgE’s to cross-link the same antigen as well, like what is shown above.


  • Yep! Mast cells are activated when IgE antibodies bind to a mast cell receptor. When IgE then binds to the one object it was designed to find, you get mast cell degranulation. This releases histamines along with a few other chemicals. Degranulation is our immune defense against parasites, so you got a head start for parasite defense for sure! But desensitization can be achieved, which makes IgG antibodies bind to the foreign object before IgE has the chance. I’d think this could be a possible treatment for the syndrome.

    Do you also have asthma? The same IgE’s also bind to eosinophil’s. Mast cell degranulation in the lungs leads to acute asthma, whereas when eosinophil’s join the party it causes airway remodeling, aka chronic asthma.


  • It’s no picnic, parasites are burly! The Th2 adaptive immune response for worms, our only parasite response, is only good with small initial infections. But since the side effects are relatively mild considering all parasites, it’s not a big area of focus.

    Fun fact: The same response for parasites causes allergies. You can never be allergic when it’s your first exposure either. But a less hygenic environment as a kid greatly redices the risk of developing allergies.








  • Toxoplasmosis is very intriguing, it has actually evolved alongside cats and humans for ages. While anyone with an immunodeficiency is at higher risk of severe side effects, like with any pathogen, it’s also associated with taking bigger risk. This is why a ton of motorcyclists and casino regulars test positive for the parasite. But when we were hunter gatherers, the infection was associated with bringing home bigger kills, which helped the entire tribe. Due to this, toxoplasmosis infections had sizable benefits and those with the infection often had positions of power in tribes!






  • Welp, the α2:3 receptors found thorough out the avian respiratory tract are also found thorough out their digestive tract…This is why factory farms using chicken litter (scrap bird feed + bird feathers + bird shit) to feed cattle has led to the first ever cases of avian flu in cows. If cows have it, won’t be long before pigs get it, and they’re the perfect mixing vessels as they have both α2:3 and α2:6 in their respiratory tract. This is the ideal setup for influenza’s classic reassortment mutation, which could easily lead to another pandemic. But, maybe this was your point lol



  • While SARS-CoV-2 has mutation baked into it’s replication cycle, the mechanism of mutation is rudimentary in comparison to influenza. This makes not wearing protection exponentially dumber in this scenario. Virologist estimate it’ll only take ~10 direct human infections from chickens or cows until the virus is ready for human to human transmission. We already got one on the books from a dairy farm at the end of March. The infections which occur prior to the virus adapting to humans are brutal too, as it attaches to the α2:3 receptor, which are only found deep in the human lung. Thus the wild mortality rate with these infections until the tropism shifts to α2:6, which are found thorough out our respiratory tract…