"One theory of immune regulation involves homeostasis between T-helper 1
(Th1) and T-helper 2 (Th2) activity"
This says it all.................they only have theories of how the immune system works.
Vaccines as presently given bypass Th1, stimulating Th2 reaction only..............so no full immunity as no response in Th1
"Multiple vaccinations shift this delicate balance, favouring the
development of atopy and, perhaps, autoimmunity through vaccine-induced
polyclonal activation leading to autoantibody production. An increase in
the incidence of childhood atopic diseases may be expected as a result of
concurrent vaccination strategies that induce a Th2-biased immune response."
Altern Med Rev. 2003 Aug;8(3):223-46.
Th1/Th2 balance: the hypothesis, its limitations, and implications for health and disease.
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.
But the hypothesis has major inconsistencies; human cytokine activities
rarely fall into exclusive pro-Th1 or -Th2 patterns. 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.
Experimentally, Th1 polarization is readily transformed to Th2 dominance
through depletion of intracellular glutathione, and vice versa. 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.
Th1/Th2-based immunotherapies, e.g., T-cell receptor (TCR) peptides and
interleukin-4 (IL-4) injections, have produced mixed results to date.