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Spike-mediated (CTL)-mediated immunity is NOT autoimmunity
Autoimmunity involves responses to SELF-antigen
This article is really important and draws attention to the distinction between autoimmunity and acquired T and B-cell-mediated immunity. We can define the difference using only two words: self and foreign.
I wrote these words before here:
“The thing that people are talking about with regard to injection-related spike embedded cell destruction, is not autoimmunity. It is the immune system working properly to clear cells with destroy-me flags on their surfaces.”
When the immune system detects a foreign (or non-self) antigen, it responds by generating an army of targeted immune mediators to detect and destroy the foreign entity. This is what is happening when foreign proteins, or the coding material for foreign protein production, are injected into us. In the case of the COVID-19 injectable products, this response is spike antigen specific, but again, the immune response would occur in response to ANY foreign protein. This is NOT autoimmunity.
The reason our immune systems don’t go haywire on our own proteins all the time is due primarily to something called clonal selection. Self antigen-recognizing cells are deleted in the plinko game that is the auto-reactive cell depletion center.
If any auto-reactive cells get through the plinko game board, there are systems in place in the periphery (and centralized) to ensure that if a cell does react to self proteins (or antigens - molecules capable of inducing an immune response), the reaction will be shut down quickly. Think of it like fire trucks to fires. If a small fire breaks out, there are fire trucks in place to respond to the fire and they are equipped to put it out. If the truck number gets impaired, or if enough trucks run out of water or anti-fire power, then the fire can get out of control. T regulatory cells play big roles as part of this fire fighting force.
Autoimmunity is something in its own class of problems. These problems have increased dramatically over the past 40 years and interestingly, are associated with the West.123 Epigenetic factors, pollution, metals, diet and toxins can all lead to autoimmune conditions. There are too many for me to list here (more than 80)4, but some include Type I diabetes, multiple sclerosis, lupus and rheumatoid arthritis.5
The one thing you don’t hear a lot about though is how vaccines can induce autoimmunity. They can. I reference some articles on this subject matter below.
A crash course in autoimmunity
It’s all in the name. Auto = self. Immunity = immunity. Immune response to self. Please read this for some background.
This article covers the emergence of autoimmunity as a result of breaks in tolerance. In terms of our fire truck analogy, this would equate to a lack of functioning fire trucks. The idea of an article that I reference therein6, was that the spike protein (SARS-CoV-2) was modulating or dysregulating normal T reg activity to ‘aggravate’ potential autoimmunity. They noted a “remarkable reduction in the frequency of Treg cells”.
But, that’s not the whole picture. I have also written about molecular mimicry and rang many bells on this subject matter because I have no doubt that this is a problem associated with the spike protein (folded sequence amino acids). Briefly, molecular mimicry is when a foreign antigen (protein) shares structural similarities with host antigens (proteins) whereby antibodies produced against the foreign antigen can subsequently bind to host antigens potentially leading to host-mediated self cell destruction, for example.
By the way, full homology is not required for this to happen. Epitope spreading or drift7 can occur when the immune response shifts to similar antigenic epitopes.
Also, there is something called Epitope modification or Cryptic epitope exposure and this is a wild, and potentially very problematic concept with regards to development of autoimmunity.89 Apparently, phylogenetically primitive sugar molecules can be ‘exposed’ to activate mammalian innate immune cell receptors to induce a chronic inflammatory state due to increased autoantibody production.10
Question: What the hell would happen in the realm of autoimmunity if any of the proteins in any vaccine comprised peptides that served as molecular mimics? James Lyons-Weiler has been asking (and answering) for years.15 You can read about pathogenic priming here.
Every single vaccine product on the market right now needs to be sequenced (in multiples and reproduced many times) and BLASTED to determine biological sequence information and to identify potential molecular mimics. And in the context of coding material injected in the context of transfection technology, such as modified mRNA technology (and DNA), ALL templates need to be screened for homology.16
SM Hayter et al., Updated assessment of the prevalence, spectrum and case definition of autoimmune disease. Autoimmun Rev. (2012).
Melissa H. Roberts, Esther Erdei, Comparative United States autoimmune disease rates for 2010–2016 by sex, geographic region, and race, Autoimmunity Reviews, Volume 19, Issue 1, 2020, 102423, ISSN 1568-9972, https://doi.org/10.1016/j.autrev.2019.102423.
Sadeghi A, Tahmasebi S, Mahmood A, et al. Th17 and Treg cells function in SARS-CoV2 patients compared with healthy controls. J Cell Physiol. 2021;236(4):2829-2839. doi:10.1002/jcp.30047.
Roopa Srinivasan, Alan N. Houghton, Jedd D. Wolchok; Induction of autoantibodies against tyrosinase-related proteins following DNA vaccination: Unexpected reactivity to a protein paralogue. Cancer Immun 1 January 2002; 2 (1): 8.
Vanderlugt, C., Miller, S. Epitope spreading in immune-mediated diseases: implications for immunotherapy. Nat Rev Immunol 2, 85–95 (2002). https://doi.org/10.1038/nri724
Powell, A & Black, M. (2001). Epitope spreading: Protection from pathogens, but propagation of autoimmunity?. Clinical and experimental dermatology. 26. 427-33. 10.1046/j.1365-2230.2001.00852.x.
Green R.S.; Stone E.L.; Tenno M.; Lehtonen E.; Farquhar M.G.; Marth J.D. (2007). "Mammalian N-glycan branching protects against innate immune self-recognition and inflammation in autoimmune disease pathogenesis". Immunity. 27 (2): 308–320. doi:10.1016/j.immuni.2007.06.008. PMID 17681821
Segal Y, Shoenfeld Y. Vaccine-induced autoimmunity: the role of molecular mimicry and immune crossreaction. Cell Mol Immunol. 2018 Jun;15(6):586-594. doi: 10.1038/cmi.2017.151. Epub 2018 Mar 5. PMID: 29503439; PMCID: PMC6078966.
Cohen AD, Shoenfeld Y. Vaccine-induced autoimmunity. J Autoimmun. 1996 Dec;9(6):699-703. doi: 10.1006/jaut.1996.0091. PMID: 9115571.
Klok FA, Pai M, Huisman MV, Makris M. Vaccine-induced immune thrombotic thrombocytopenia. Lancet Haematol. 2022 Jan;9(1):e73-e80. doi: 10.1016/S2352-3026(21)00306-9. Epub 2021 Nov 11. PMID: 34774202; PMCID: PMC8585488.
Guimarães LE, Baker B, Perricone C, Shoenfeld Y. Vaccines, adjuvants and autoimmunity. Pharmacol Res. 2015 Oct;100:190-209. doi: 10.1016/j.phrs.2015.08.003. Epub 2015 Aug 12. PMID: 26275795; PMCID: PMC7129276.
Lyons-Weiler J. Pathogenic priming likely contributes to serious and critical illness and mortality in COVID-19 via autoimmunity. J Transl Autoimmun. 2020 Apr 9;3:100051. doi: 10.1016/j.jtauto.2020.100051. PMID: 32292901; PMCID: PMC7142689.
Salemi S, D'Amelio R. Could autoimmunity be induced by vaccination? Int Rev Immunol. 2010 Jun;29(3):247-69. doi: 10.3109/08830181003746304. PMID: 20521925.
Shoenfeld Y, Aron-Maor A. Vaccination and autoimmunity-'vaccinosis': a dangerous liaison? J Autoimmun. 2000 Feb;14(1):1-10. doi: 10.1006/jaut.1999.0346. PMID: 10648110.
Tishler M, Shoenfeld Y. Vaccination may be associated with autoimmune diseases. Isr Med Assoc J. 2004 Jul;6(7):430-2. PMID: 15274537.
Molina V, Shoenfeld Y. Infection, vaccines and other environmental triggers of autoimmunity. Autoimmunity. 2005 May;38(3):235-45. doi: 10.1080/08916930500050277. PMID: 16126512.
Geier MR, Geier DA. A case-series of adverse events, positive re-challenge of symptoms, and events in identical twins following hepatitis B vaccination: analysis of the Vaccine Adverse Event Reporting System (VAERS) database and literature review. Clin Exp Rheumatol. 2004 Nov-Dec;22(6):749-55. PMID: 15638050.
Warkentin TE. Platelet-activating anti-PF4 disorders: An overview. Semin Hematol. 2022 Apr;59(2):59-71. doi: 10.1053/j.seminhematol.2022.02.005. Epub 2022 Feb 20. PMID: 35512902.