Figured it out!
I GOT IT!!:victory: And I was sort of right the first time, I just wasn't explaining it well because I was explaining the theory of CYTOTOXIC cells (CD8+ T cells), and then we got talking about CD8 the suppressor cell, and it was all downhill from there! I got confused with the names, but my theory was on the right track. The confusion is MY FAULT because I was erroneously TYPING CD8 for short, not realizing there was a difference in their actions. I knew what I was talking about, just couldn't convey that in a way that made sense because we were using the same names for 2 different things.
CD8 is just one type of a suppressor cell, but the "CD8+ T cell" is a
cytotoxic T-lymphocyte. Big difference!
http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/B/B_and_Tcells.html
"The best understood CD8+ T cells are cytotoxic T lymphocytes (CTLs). They secrete molecules that destroy the cell to which they have bound."
"In general, the role of the CD8+ T cells is to monitor all the cells of the body, ready to destroy any that express foreign antigen fragments in their class I molecules."
http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/C/CTL.html
"Cytotoxic T lymphocytes are
lymphocytes that kill other ("target") cells."
"Targets may include:
* virus-infected cells (e.g., HIV-infected CD4+ T cells)
* cells infected with intracellular bacterial or protozoal parasites
* allografts such as transplanted kidney, heart, lungs, etc.
* cancer cells (The tumor-infiltrating lymphocytes, TIL, that have shown some promise in cancer therapy contain CTLs."
"
There is also evidence that CTL are active in some autoimmune disorders, e.g. help destroy the beta cells of the islets of Langerhans, leading to Type I diabetes mellitus."
"Properties of CTLs: Most of them belong to the CD8+ subset of T cells."
So I'll go back to my original theory, but use the correct terminology -- My
CD8+ T cells are too high. They are attacking things they don't need to attack because my immune system is OVERACTIVE. It's being overstimulated. For example, I had the flu in September. My CYTOTOXIC cells attacked the flu virus, but didn't stop there. I had 4 illnesses back to back that month, including that flu, shingles, viral stomatitis, and another flu-like illness. Because once my CYTOTOXIC CELLS were activated by flu virus, they kept going. During an illness or infection, HISTAMINE is released, and
histamine ACTIVATES the T SUPPRESSOR CELLS to secrete LYMPHOKINES, which are responsible for the flu-like symptoms. Lymphokines amplify the INFLAMMATORY response. If you have too many lymphokines, you will have an exaggerated inflammatory response. Lymphokines attract macrophages and other lymphocytes and ACTIVATE them to start fighting. (In MY CASE, I didn't NEED them to fight, they were targeting things they didn't need to target.) So now the immune system is in full attack mode, you have all this inflammation, and it's waking up latent infections, and you feel SICK. Your body reacts with a fever, chills, swollen lymph nodes, body aches, and FATIGUE. (Sound familiar yet?)
T suppressor cells have H2 receptors on their cell surfaces, activated by histamine --
activated to release lymphokines, that is. Activated to CONTINUE the inflammatory response which is making you feel ill. Tagamet is an H2 BLOCKER, so it is thought that it INACTIVATES the T suppressor cell's ability to release more lymphokines, MODULATING the immune reaction.
http://books.google.com/books?id=Finslj9ZUaoC&pg=PA196&lpg=PA196&dq=CFIDS+and+Tagamet&source=bl&ots=om0sHFh3nJ&sig=etQBV9EaF8UGY9M3P6QgkcORmLM&hl=en&ei=TY9kS5PkK4ihlAe3qJCUCg&sa=X&oi=book_result&ct=result&resnum=2&ved=0CA0Q6AEwAQ#v=onepage&q=CFIDS%20and%20Tagamet&f=false
"Dr. Goldstein's rationale for treatment was based on the fact that Epstein Barr virus, which causes mononucleosis, is a herpesvirus and, in most herpes infections, there is an increased number of T suppressor cells. It had been recently demonstrated that the cells were activated by histamine. Dr. Goldstein reports positive results in 90% of cases of mononucleosis treated with Tagamet."
"Although the cause of CFIDS remains undetermined, it is known there is activation of T suppressor cells, probably due to viral activity. It is believed that the H2 blockers inhibit overporduction of lymphokines responsible for some of the flu-like symptoms of CFIDS."
You can look at it by another mechanism as well, which is where most of you are focusing, and that is inhibiting the T cells from shutting down prematurely. You're inactivating the T suppressor cells so your body can effectively fight off the infection. Either way, whether you're preventing them from shutting down too soon, or you are inhibiting the amount of lymphokines they secrete when activated by histamine -- it still works. You guys were right in your theory, and I was right in my theory, I just didn't explain it very well! In my defense, my theory is way more complicated than yours. :Retro tongue: But I knew what I meant in my head (that counts for something, right?) and bottom line -- the Tagamet works. It works in many ways, and all of them are beneficial to me. It helps my modulate my overactive immune system, and it enhances my body's ability to suppress the latent infections. I'm sold.
And this also explains why you may need to be more aggressive with Tagamet if you have a weak immune system, and why I need LESS because I have an overstimulated immune system. It all comes together now. So with that being said, those with autoimmune symptoms might want to take a more conservative approach.
