..."There is an inflammatory process going on that seems to have been triggered by something - that process started to affect other parts of the body so we have two jobs to do," he said.
"One is to try to treat the inflammation and the other is to deal with the consequences of it."
"...An investigation by New Scientist suggests the drug may have caused a super-immune response – sending white blood cells called T cells rampaging through the body destroying its own tissues. ..."
....The increase in "bacterial" infection. BAD news!! I researched further. The particular "bacterial" infections that are connected with inhibited IL-2 are from "superantigens". In other words, things like TB, borrelia, systemic infection, toxic shock, sepsis, things like that. MANY bacterial infections in the world, as you know, are already becoming resistent to antibiotics, and death often happens pretty quickly. And many of these everyday bacteria that we all are exposed to are held in check in everybody's body by our immune system. Bottom line, held in check by IL-2. And this concern doesn't even take into consideration what we already know is the risk that is being run, when being treated with immunosuppressants, from the possible increase or activation of viral infections. ...
...Messing with IL-2 can be nasty. Real nasty. Again, in organ rejection, it can be and is needed under very close monitoring (it is even suggested via hospitalization) and most often for short-term use. But in or for a basically non-fatal disease like MS? Pardon my scoff, but...........yeah, right!!! ...."
...Yea, usually IL-4 and IL-10 work in concert (at least that's what I found from my reading habits..... ), but they aren't dependent upon one another, which I believe is a good thing in MS for purposes of immune modulation.
The thing is, in MY opinion (and I ran across this while researching the drug desipramine and hence why I went off on sidelines regarding individual cytokines) that you want to raise levels of IL-10 (anti-inflammatory, and it helps to reverse the blood/brain barrier permeability); but lower levels of IL-4 for reasons of inhibiting CD4 attacks on myelin, and IL-4 enhances MHCII binding (APCs), so again, keeping IL-4 lower should (note I say "should", this again is totally unproven, and still controversial) also be adjunctive and beneficial because you definitely want to regulate MHCII. Higher levels of IL-4 correlates with lymphoma, also. Keeping IL-4 on the low end (or perhaps maintaining status quo levels of IL-4 in MS, once it is determined what the optimum levels of IL-4 should be in MS) helps to maintain or increase VIP. Without going into another long dissertation about VIP/PACAP, I'll quote from my original research: VIP/PACAP contributes to the initiation of TH2-type immunity, whereas in the presence of a full-blown, inflammatory reaction, VIP/PACAP act as anti-inflammatory agents.
Keeping the immune system predominantly on the TH2 side of the equation is desirable (from what I can find) in MS (whether that holds true in ALL patterns of MS, is yet to be determined).
Ok....here's the odd part about IL-4. There ARE different suppositions about IL-4 in MS. Copaxone, for one, raises levels of IL-4 and IL-10. Interferon appears to maintain or decrease levels of IL-4. The problem with the interferons in my mind (which is another topic of discussion) is that it was found that over time IFN-beta 1b also increases some pro-inflammatory cytokines, IL-6 for one, which is part of the problem that contributes to the side-effects, and apparently could potentially counteract its beneficial immunomodulatory effects. Odd, huh?
I found that desipramine decreases (or maintains) IL-4 and increases IL-10. Both, in MY sole opinion, to be desirable for MS treatment (or therapy, if it can ever be ascertained via clinical trials on MS).
Plus, this is only pertaining to the immune side of the equation in MS (or some forms of MS). The genetic, environmental toxin, and pathogen sides, which are also pieces of this complex puzzle, aren't even factored in with this.
I still say to clinical researchers everywhere: Do an ELISPOT on each of your MS patients periodically, so we can correlate the findings and see what we come up with! That just MIGHT weed out a few, anyway, of the ongoing theories over cytokines and MS, correct?...
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