170620- Email re Allen Steere talking about deformed (transformed) B cells

To: Senate Judiciary Committee Staff and Others

Cc: The Lobbying Crew

Subject: Lyme Cryminal Allen Steere talking about deformed B cells (also caused by the OspA fungal vaccines)

Date: Jun 20, 2017 7:42 AM

 

Greetings,

I dont know if you saw this or knew this history (we showed you in our meetings and within our handouts that Allen Steere falsified the case definition, such that now you can only have “Lyme disease” if you are “not sick and only have an autoimmune bad knee”) regarding how Allen Steere knew Lyme and LYMErix were an immunosuppression outcomes (the opposite) and a B cell mutation disorder.

 

When the B cells are “immature” and “Epstein-Barr-like deformed,” they are not really doing their jobs. Hence, what we have is an AIDS like disease. And you all will remember AIDS is about the reactivation of latent herpesviruses producing the likes of Karposi’s sarcoma (caused by a herpesvirus).

I think it is important for you all to see this with your own eyes and see that indeed, Allen Steere is an author of this report:

 

Remember, OspA is Pam3Cys…

Ann N Y Acad Sci. 1988;539:65-79.

Clinical pathologic correlations of Lyme disease by stage. Duray PH1, Steere AC.

”….Soon after the onset of ECM, the organism disseminates hematogenously, with what appears to be random dispersal throughout the body. The immune response involves virtually all of the organs and structures of the reticuloendothelial system including the bone marrow, and clinical pain and discomfort seems to correlate with hyperplasia of lymph nodes and spleen and bone marrow. Diffuse visceral involvement in this acute stage mimics infectious mononucleosis or disseminated viral syndromes. These include conjuctivitis, pharyngitis, pneumonitis with dry cough and mild pleuritic pain, hepato-splenic tenderness, lymph node swelling of the neck and groin, and orchitis. There is lymphoid hyperplasia of the lymph nodes and spleen consisting of prominent germinal centers and numerous perifollicular lymphocytes, with proliferation of plasma cell precursors and mature plasma cells. The plasma cell precursors are large, appear tumor-like, and can resemble Reed-Sternberg cells. Others look like typical immunoblasts (FIG. 1). In one example, cervical lymph nodes show cell degeneration with karyorrhexis and nuclear debris of lymphoid elements. This patient had repeated high fevers and marked discomfort of neck nodes. Large atypical immunoblasts can also be seen in the spleen and bone marrow. The red pulp of the spleen is congested, not unlike that seen in infectious mononucleosis. Spirochetes can be demonstrated in the lymph nodes, spleen and bone marrow and liver. There is a transient hepatitis reflected by elevated liver cell enzymes such as SGOT, SGPT, and GGT. The liver can vary from a mild lymphocytic portal triaditis all the way to liver cell derangement that simulates acute viral hepatitis. The cells at this stage appear swollen with clear cytoplasm and microvesicles of fat (FIG. 2). Numerous leukocytes are seen in the sinusoids, and there is Kupffer cell hyperplasia…” https://www.ncbi.nlm.nih.gov/pubmed/2847622

http://www.actionlyme.org/clinical-pathologic-correlations-of-lyme-disease-by-stage-Steere-Duray.pdf —-

 

 

And, see Pam3Cys (same antigen as OspA, LYMErix vaccine): J Immunol. 2005 Jun 1;174(11):6639-47.

Role of TLR in B cell development: signaling through TLR4 promotes B cell maturation and is inhibited by TLR2.

Hayashi EA1, Akira S, Nobrega A. Author information Abstract

The role of TLR4 in mature B cell activation is well characterized. However, little is known about TLR4 role in B cell development. Here, we analyzed the effects of TLR4 and TLR2 agonists on B cell development using an in vitro model of B cell maturation. Highly purified B220(+)IgM(-) B cell precursors from normal C57BL/6 mouse were cultured for 72 h, and B cell maturation in the presence of the TLR agonists was evaluated by expression of IgM, IgD, CD23, and AA4. The addition of LPS or lipid A resulted in a marked increase in the percentage of CD23(+) B cells, while Pam3Cys had no effect alone, but inhibited the increase of CD23(+) B cell population induced by lipid A or LPS. The TLR4-induced expression of CD23 is not accompanied by full activation of the lymphocyte, as suggested by the absence of activation Ag CD69. Experiments with TLR2-knockout mice confirmed that the inhibitory effects of Pam3Cys depend on the expression of TLR2. We studied the effects of TLR-agonists on early steps of B cell differentiation by analyzing IL-7 responsiveness and phenotype of early B cell precursors: we found that both lipid A and Pam3Cys impaired IL-7-dependent proliferation; however, while lipid A up-regulates B220 surface marker, consistent with a more mature phenotype of the IgM(-) precursors, Pam3Cys keeps the precursors on a more immature stage. Taken together, our results suggest that TLR4 signaling favors B lymphocyte maturation, whereas TLR2 arrests/retards that process, ascribing new roles for TLRs in B cell physiology. https://www.ncbi.nlm.nih.gov/pubmed/15905502

 

The short version is, this crime is easily prosecutable because we are quoting the criminals, and so in the witness stand they all can be asked, “Did you publish this? Did you publish this? Did you publish this?…”

They cant very well say they were mistaken about every aspect of this that they did a 180 on.

 

Kathleen Dickson
ActionLyme.org and TruthCures.org

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