TLR4 and MyD88. These have been discussed at length in my threads dealing with the CYTOTOXIC nature of the SPIKE PROTEIN. There is a parallel scenario which involves these very same proteins and genes. TLR2 or TLR4 deficiency alone or Myd88 deficiency restricted to either donor or host was not sufficient to prevent rejection.
Cell damage or death associated with the transplantation procedure releases a large variety of ‘danger’ molecules that potentiate rejection.
What is interesting is that drugs against HLA antibodies, such as Rituximab and Bortezomib, post transplantation ENHANCE coronavirus disease in mice and COVID-19 in humans. Whilst drugs against alloimmunty, such as Alemtuzumab, are highly effective.
The immense peptide sharing of the spike protein may mimic injection of self-peptides, which has proven fatal in mice.
Is this why the virus MIMICS ALLERGY?
DOES THE SPIKE PROTEIN MAKE US ALLERGIC TO OURSELVES?
Anti-peptide autoantibodies and fatal anaphylaxis in NOD mice in response to insulin self-peptides B:9-23 and B:13-23
The Proteasome Inhibitor Velcade Enhances rather than Reduces Disease in Mouse Hepatitis Coronavirus-Infected Mice
Cases of COVID-19 in Alemtuzumab-Treated Patients With MS: Pharmacovigilance Report (2059)
The Innate Immune System in Transplantation