Funny - Several of us are on the same page regarding TH1/ TH2 balance.
Don't know if these will help but here are some excerpts, quotes and my personal notes from the background research that I am currently doing for an opinion paper.
* Th2 activated. In a simplified nutshell, this means you over-respond to toxins, allergens, normal bacteria and parasites, and under-respond to viruses, yeast, cancer and intracellular bacteria (such as Chlamydia/mycoplasma). Allergies, asthma, eczema are examples of Th2 activated diseases. IL 10 tends to be the primary cytokine activated.
* [b]Th1 activated[/b]. Also, in a simplified nutshell - This means you over-respond to virus, yeast, cancer and intracellular bacteria and under-respond to toxins, allergens, normal bacteria and parasites. [b]MS is generally considered to be Th1 activated as are Rheumatoid Arthritis and IBD. [/b] IL 12 tends to be the primary cytokine and there tends to be a perfusion of macrophages and Tlymphs.
* The immune system has two different modes of attack, based on the type of invader. One is Th1 (T Helper 1). It goes after organisms that get inside our cells ‚ intracellular pathogens. It is also known as cell-mediated immunity. The other is Th2 (T Helper 2). It attacks extracellular pathogens ‚ organisms that are found outside the cells in blood and other body fluids. Some call this humoral or antibody-mediated immunity. A healthy immune system is dynamic, able to switch back and forth as needed, quickly eradicating one threat and then resting before responding to the next.
* Viruses, especially herpes viruses like EBV, CMV and HHV6, can make proteins that mimic IL-10. The virus which should be handled by a Th1 immune response tricks the immune system into acting as if the threat needs a Th2 response. So the immune system shifts from an appropriate Th1 mode that attacks viruses to the Th2 mode that is weak and ineffective against viruses. The virus increases its chances of survival by diverting the immune system.
It is now thought that many, if not most, pathogens have this ability. For example, you get a parasite which should be handled by a Th2 response. The parasite however produces as part of its will to live defense an IL-12 like molecule, which fools your immune system into thinking the threat is coming from a virus, yeast or intracellular bacteria. The fake IL-12 causes your immune system to shift from the TH2 response that would go after the parasite, to the TH1 response, which does little if anything to parasites. Points for the helminth's are good for MS'ers theory.
• [b]Elevation of cortisol is also known to suppress Th1 cell-mediated immunity and to cause a shift to the Th2 type of immune response. [/b]. Several mechanisms are involved, including suppressing the secretion of IL-1 by macrophages, inhibiting the differentiation of monocytes to macrophages, inhibiting the proliferation of T lymphocytes, and increasing the production of endonucleases, which increases the rate of apoptosis of lymphocytes . Could this be why the folks successfully experimenting with bee venom therapy see their success? Does it shift/attempt to balance the immune system from a Th1 response to a Th2 response?
*The protective effect of pregnancy on putative Th1-mediated autoimmune diseases, such as multiple sclerosis and rheumatoid arthritis, is associated with a Th1 to Th2 immune shift during pregnancy. The hormone estriol increases during pregnancy and has been shown to ameliorate experimental autoimmune encephalomyelitis and collagen-induced arthritis.
* Th1/Th2 imbalance is hypothesized to up-regulate some diseases and down-regulate others. Compared to controls, multiple sclerosis (MS) (Th1-mediated) has been linked to a reduced risk of allergy and asthma (Th2-mediated), based on patient questionnaire studies and a review of asthma medication.
*One theory of immune regulation involves homeostasis between T-helper 1 (Th1) and T-helper 2 (Th2) activity. The Th1/Th2 hypothesis arose from 1986 research suggesting mouse T-helper cells expressed differing cytokine patterns. This hypothesis was adapted to human immunity, with Th1- and Th2-helper cells directing different immune response pathways. Th1 cells drive the type-1 pathway ("cellular immunity") to fight viruses and other intracellular pathogens, eliminate cancerous cells, and stimulate delayed-type hypersensitivity (DTH) skin reactions. Th2 cells drive the type-2 pathway ("humoral immunity") and up-regulate antibody production to fight extracellular organisms; type 2 dominance is credited with tolerance of xenografts and of the fetus during pregnancy. Overactivation of either pattern can cause disease, and either pathway can down-regulate the other.
[b]But the hypothesis has major inconsistencies; human cytokine activities rarely fall into exclusive pro-Th1 or -Th2 patterns. [/b]The non-helper regulatory T cells, or the antigen-presenting cells (APC), likely influence immunity in a manner comparable to Th1 and Th2 cells. Many diseases previously classified as Th1 or Th2 dominant fail to meet the set criteria. [b]Experimentally, Th1 polarization is readily transformed to Th2 dominance through depletion of intracellular glutathione, and vice versa.[/b] Mercury depletes glutathione and polarizes toward Th2 dominance. Several nutrients and hormones measurably influence Th1/Th2 balance, including plant sterols/sterolins, melatonin, probiotics, progesterone, and the minerals selenium and zinc. The long-chain omega-3 fatty acids EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) significantly benefit diverse inflammatory and autoimmune conditions without any specific Th1/Th2 effect.
* Also MS patients secreted increased amounts of IL-4 and IL-10 and decreased quantities of TGF-beta. TGF beta controls proliferation, differentiation, and other functions in most cell types. Thus, these studies suggest that there is a dysregulation in the balance between pro-inflammatory Th1 and anti-inflammatory Th2 cytokines in MS. It appears that the presence of Th1 secreting autoreactive T cells in healthy individuals may be counterbalanced by the presence of cells secreting Th2 cytokines and by the augmented production of the immunosuppressive cytokine TGF-beta, whereas in MS there is a decrease in these anti-inflammatory agents.