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There are three avenues of tolerance
- Clonal Deletion
- Clonal Anergy
It appears to me, the only avenue to fix a food allergy is through immunoregulation (see the “Not A Solution” sections).
Induce iTreg formation through low dose allergin in combination with Treg upregulators to reduce and remove learned allergies.
- Ensure no systemmic inflammation
- Ensure adequate vitamin A and vitamin D
- Prior to meal
- Take a histone/protein deacetylation inhibitor (Sodium Butyrate, 600mg)
- Take Colostrum (1 Tbls liquid, 1 tsp powder) (raw will be more effective) (see colostrum section)
- With a meal, take a small amount of the allergin (less than would cause any allergy symptoms)
- Repeat above for 2 weeks
- Test for allergy by taking minimum amount of allergin that would cause symptoms. If not symptoms, it may be wise to continue the protocol for another 2 weeks to ensure sufficent elimination of reactive immune cells
Lactoferrin [LF] is an endogenous anti-inflammatory pleiotropic protein secreted at high concentrations in colostrum and at mucosal sites.
[VEN-120, a Recombinant Human Lactoferrin ] reduced inflammation in both models of IBD, accompanied by increased Tregs in the intestinal lamina propria
MicroRNA-148a directly downregulates the expression of DNMT1
DNMT1 deficiency results in highly efficient FoxP3 induction
Boiling of cow’s milk results in substantial loss of microRNA148a-3p
There is a good article explaining the dynamics and supplements for this here https://selfhacked.com/blog/oral-tolerance/ , and information genenerally about Tregs here https://selfhacked.com/blog/treg/
The good news is that HDAC inhibitors such as Butyrate block the conversion of healthy Tregs to IL-17 producing Tregs (R).
The Role of Regulatory T Cells in IgE-Mediated Food Allergy
Recent findings demonstrate that oral tolerance can be induced in the tonsils through generation and maintenance of functional allergen-specifi c Treg cells
Clonal Deletion Not A Solution
This occurs prior to maturation. It does not account for presently reactive immune cells.
Anergy Not A Solution
There’s no assurance that APCs will not present the antigen before T Lymphocyte encounterance
Thus when an antigen is properly presented to the T lymphocytes by an antigen presenting cell (APC), which displays the antigen on its MHC II complex and which activates T cell´s costimulatory receptors, T lymphocytes undergo productive response. However, when T cells interacts with an antigen not presented by the APCs, that is very probably not the antigen that an immune response should be held against, the T cell undergoes anergy – https://en.wikipedia.org/wiki/Clonal_anergy
Even if anergy were an options, there are multiple issues:
Chronic exposure of peripheral B cells to HEL (serum levels greater than 10–20 ng/ml) results in anergy, as defined by unresponsiveness to antigen stimulation
It has been shown in both anti-HEL and Ars/A1 models that maintenance of anergy requires constant binding of antigen to BCR
In otherwords, not only would you have to ensure some serum level of the antigen for some chronic period, you would have to continue to do so or else the anergy would reverse.