YOU HAVE MAST CELL TROUBLE, EXCESS ALLERGIES, HIGH INFLAMMATION AND AUTOIMMUNITY AND...
WHY I AM REACTING TO EVERYTHING-10 MORE REASONS
First, about 20 years ago, before a hot topic, Dr. Gary Rosen, and a few seasons before him, R. Shoemaker, involved me in 3 mold medicine books. They had very different skill sets, and thanks to Dr. Rosen, the author of the highest number of mold science textbooks in print and master builder, if HE remediates a location, the issue is not eternal--for the last 20 years.
BUT MANY OTHER REASONS FOR ONGOING SENSITIVITY are summarized below on brain antibody issues (AI).
- Cleaning the blood by plasma electrophoresis showed that some patients had a drop in autoimmunity against neuron chemicals over 2 months. Others showed no improvement and the antibodies against brain tissue stayed the same.
- The removal of circulating immune complexes,
- complement components,
- cytokines [vast numbers of inflammatory or anti-inflammatory chemicals
- adhesion molecules;
- the replacement of missing blood plasma components;
- Alteration of the numbers of immune cells and the function of regulatory T cells (Treg) and natural killer cells;
- Sensitization of antibody‐producing cells to immunosuppressant agents. 16 , 17 , 18
--------------------------- A few other thoughts from the research----------------------
Prior studies have evaluated the role of cytokines/chemokines in AE. [Autoimmune Encephalitis]
Anti‐NMDARencephalitis patients showed distinct CSF interleukin‐17 (IL‐17)A/IL‐6 axis activation, which might promote intrathecal antibody synthesis, resulting in delayed responses after immunotherapy. 19
Serum IL‐17 and IL‐23 titers were increased in patients with cell surface antibody‐associated AE compared to patients with other CNS inflammatory diseases or healthy controls,
and the cytokine titers correlated with antibodies. 20
Furthermore, a study reported that the titers of CXCL13 were increased in the CSF of anti‐NMDAR encephalitis patients and that the chemokine titers correlated with intrathecal antibody titers, treatment response, and relapse. 21
The studies suggest that cytokines/chemokines play a vital role in AE, although subtype-related alterations have not been evaluated. 19
SOURCE: Ann Clin Transl Neurol. 2021 Apr; 8(4): 763–773.
Published online 2021 Feb 20. doi: 10.1002/acn3.51313
PMCID: PMC8045938. PMID: 33609012
Clinical efficacy of plasma exchange in patients with autoimmune encephalitis
Yan Zhang, corresponding author 1 Hui‐jin Huang, 1 Wei‐bi Chen, 1 Gang Liu, 1 Fang Liu, 1 and Ying‐ying Su 1