Th2 AKTIVOITUMINEN

[Bb]

Lähettäjä: Soijuv Lähetetty: 12.11.2004 16:02

Clark sairasti itse borrelioosia - hän on parantanut itsensä ja muitakin borrelioosia sairastavia moduloimalla immuunijärjestelmän toimintaa. Hän aktivoi Th2 eli vasta-ainevälitteistä immuniteettia artikkelissa mainituilla valmisteilla:


VÄITÖSKIRJA: Steven Clark, ND375 N. Main Street Wolfeboro, NH 03894
603-569-5545

(He had Lyme and has treated 7 others with Lyme for 10 yrs. or longer and are all doing well.)

The point is that the antibodies are effective. The ones that get the autoimmune consequences are the ones that stay stuck in TH-1. Macrophages can be active without antibodies. There are no" holes" in antibodies. They either stick strongly, weakly or none TNF is a TH3 response (not a th1)response."

Immunologic Considerations
MHC
Major histocompatibility complex (MHC) class II activate. The configuration and sequence of the MHC II molecule determines what antigens will fit onto MHC II antigen presenting cells. Second , MHC II molecules induce the thymus to regulate the developmental selection of T-cell-receptor specificity toward individual antigens.

MHC II molecules have been implicated in various forms for immune dysfunction. Patients with antibiotic resistant LD often have the HLA-DR4 allele on helper T cells, the same allele as patients who have rheumatoid arthritis. One feature of LD autoimmune arthritis is a predominant presentation of Bb antigen in the HLA-DR2 allele of MHC II. About 15% of patients with chronic arthritis resistent to multiple couses of antibiotics present Bb antigen in the HLA-DR2 or HLA-DR4 MHC II haplotypes. These patients are gentically susceptible to long term arthritis even after Bb can no longer be found in the synovical tissue.

Cross reactivity
Molecular mimicry exists between Bb fagella antigens and human axons, myelinated fibers of peripheral nerves, joint synovia, heart muscle, myosin and human mitochondrial proteins and T cell MHC alleles. Some HLA-DR2 and HLA-DR4 positive individuals demonstrate high levels of IgG to a small portion of OspA surface protein of Bb with OspA-specific T helper 1 (Th-1) cells. These T cells are located in the synovial tissue of the host. A 12 amino acid sequence of this OspA epitote region cross-reacts with Human lymphocyte function associate antigen-1 (LFA-1).Th-2 stimulation is dependent on the LFA-1. This appears to be the mechanism the Bb alters the host immune response.

Antibody Reaction

Bb can be removed from the blood quickly with an appropriate antibody response. Specific IgM and IgG antibodies can agglutinate Bb, which is then destroyed via complement-mediated lysis.

During stage II, Bb is phagocytosed by macrophages via host antibody/Tcell interaction. Bb can hide from the antibody response by binding to a component of myelin, locating deeper tissues,altering their outer envelope markers through gene rearrangement.Bb can also move into the tissues with low blood supply where oxygen saturation is reduced and antibodies can not reach.

IgM first appears two to four weeks after the appearance of ECM, peaks six to eight weeks and then declines to normal four to six months. At the time of ECM presentation 35% of patients will be IgM positive,24% will be IgG positive.

IgG appears six to eight weeks after onset. IgG peaks at four to six months. The IgG levels may decline after treatment, but usually remain detectable for years after infection, regardless of treatment efficacy or presence of remaining organisms. For this reason, antibody levels can not be used to determine effectiveness of treatment.

The first antibody is directed toward flagellin antigen. Anti Osp-C antibody appear early in some individuals. Later, at least 11 different epitopes are involved including High titered IgG aOsp-A and aOsp-B Bb surface antigens in 50% of patients.

20% of patients treated with antibiotics during stage I with ECM will not develop antibody response. The remainder will be seropositive 8 to 12 days from treatment onset.

T Helper subset 1/T helper subset 2 balance

CD4 positive(DC4+) T helper (Th) cells modulate a proper immune response. CD4+ cells are subdivided into two functionally distinct subgroups identified historically by their cytokine secretion profiles. The dominant CD4+ cytokine profile dtermines the immune response.

The Th-1 cytokine complex of IFNy, TNFB, interleukin-2 (IL-2) and IL-12. Th-1 CD4+ cells are responsible for intitating cell mediated immunity by activating cytotoxic cells, inflammatory components, initiating delayed hypersensitivity reactions and stimulating sIgA, which supports mucosal immunity.IL-4 and IL-10 (Th-2) down regulates the Th-1 response.

The Th-2 cytokine complex of IL-4,IL5,IL6,IL-9,IL-10 and IL-13. Th-2 CD4+ cells are responsible for most immunoglobulin production, antibody class switching from IgG to IgE and activation of eosinophils. IFNy and IL-12 (TH1) down regulates the Th-2 response.

Autoimmunity is a consequence of inappropriate Th-1 or Th-2 dominances, when either subset becomes locked into an active state. If an individual's T cell subset is predominately Th-1 at the time of Bb infection, the organism can cause the host's immune system to lock into the Th-1 subset. If the host in a cell mediated immunity phase, Bb can prevent the host from immunologically switching to antibody production. Synovial fluid mononuclear cells in LD arthristis promote a Th-1 pattern with high levels of TNFB,INFy and little or no IL-4. Measurement of cytokines may be the only way to determine which Th cytokine profile is dominant.

Antibody reaction to LD is the major protective mechanism for humans. Cell mediated immunity plays no demonstrable defensive role and seems to exacerbate destructive arthritis. Despite the necessity to activate an antibody response, only 88% of patients diagnosed with LD have either IgM or IgG. Therefore Bb creates an advantage by reducing host antibody response. This is accomplished by altering the Th-1/Th-2 balance. Bb modulates the immune system toward the Th-1 response, when a Th-2 antibody response with what is necessary to fight the infection and avoid autoimmune reaction.

Conclusion
Lyme disease is a complicated, multistage, potentially crippling disease. It is essential that the healing community continue to perfect diagnosis and treatment of this destructive illness. Prevention is the first line of defense. Rapid diagnosis is ideal to reduce long term effects by allowing for appropriate, timely treatment. Long term arthitis, the most common destructive sequelae of LD: can be avoided with immunologic treatment protocols aimed at re-modulation of the Th-1/Th-2 balance. Research must consider methods to remove the risks of autoimmune consquences.

General Treatment Approach
Theoretical treatment goals:

To stimulate the Th-2 response by stimulation of endogenous or exogenous IL-10 and IL-4.

To avoid stimulatimg Th-1 cytokines.
To re-balance the immune system after the immune system is remodulated.

T-helper subset cells develop according to the cytokine profile present when stimulated. Therefore it is critical to intervene early and create a Th-2 Dominance.

Improve Th-2 response

Supplements:
-Stimulate endogenous glucocorticoids
-Elderberry
-Streptococcus thermophilus, Bifida bulgaris, and Bifida biidum.
-phosphatidylcholine containing arachidonic and stearic acids
-1,25-dihydroxyvitamin D3
-Vitamin A, high dose short term.
-soluble CD-30 glycoprotein from colostrum
-Astragalus membranaceus, Echinacea augustfolia
-cold pressed soybean,corn,safflower and canola oil.

Avoid :
-Alcohol
-exogenous corticosteroid
-Reduce Omega 3 fatty acids
-L. plantarum and L. casei
-silica in food and supplement form
-Panax ginseng
-Chlorella
-Neem
-garlic
-Melatonin
-dihydroepiandrosterone
-Ultraviolet light avoid UVA
-Avoid UVA
-Avoid vitamin E
-Lentinian
-Ginko biloba
-curcumin
-Angelica sinensis
-Withania somnifera
-Eupatorium perfoliatum, Glycyrrhiza glabra,Ligustrumlucidum,Taraxicum officinale.

The Vitamin E Induces IL-2, natural killer cell function,IFNy. Vitamin E also decreases IL-4 and IL-6, especially in elderly patients.

The Garlic activates NK cells, increases T cell function and increases levels of IL-2.

Chlorella increases the expression of IFNy,IL-2 and increases macrophage activation.

Other treatment options:

Deer Antler
The syphilitic Miasm
Teasel Root
Hyberbaric Oxygen Therapy
Castor Oil packs