Steere and Pseudolymphoma from Lyme and LYMErix; “Reed-Sternberg Cells”

 

Check it out.  See the Wikipedia page on these types of cells that Steere saw in Lyme victims in 1988 and compare that with what Nicole Baumgarth showed is an outcome of Lyme in 2015.  It looks like the answer will come from oncology.

See, Truth Cures… get it?  Your “LLMD” does not know anything about this.  See the charge sheets so you can be more informed than “doctors” and you can then start charging THEM for your time.

And by the way, that’s about to be true; a PA judge has decided a person diagnosing herself with Lyme is equal to a doctor diagnosing her with MS, which means in the eyes of the “court,” a non-doctor’s opinion weighs the same as a doctor’s.  Start charging them for your time and expertise.  Here is that story:
http://www.thelegalintelligencer.com/id=1202796067890/Pa-Justices-Agrees-to-Eye-Facebook-Posts-Impact-on-Discovery-Rule

 

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

170822_STEERE_IMMUNOBLASTS

This is ^^^ by Allen Steere, remember, who now says you dont have Lyme unless you have bad knees only.

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FROM WIKIPEDIA (see especially where I italicized):

“Reed–Sternberg cells (also known as lacunar histiocytes for certain types) are different giant cells found with light microscopy in biopsies from individuals with Hodgkin’s lymphoma (a.k.a. Hodgkin’s disease, a type of lymphoma). They are usually derived from B lymphocytes, classically considered crippled germinal center B cells, meaning they have not undergone hypermutation to express their antibody. Seen against a sea of B cells, they give the tissue a moth-eaten appearance.[1]

“Classification of Hodgkin’s is based on the reactive cell mixture. Immunomarkers are used (e.g., CD15 and CD30).

“Reed–Sternberg cells are large 30–50 microns and are either multinucleated or have a bilobed nucleus with prominent eosinophilic inclusion-like nucleoli (thus resembling an “owl’s eye” appearance). Reed–Sternberg cells are CD30 and CD15 positive, usually negative for CD20 and CD45. The presence of these cells is necessary in the diagnosis of Hodgkin’s lymphoma – the absence of Reed–Sternberg cells has very high negative predictive value. They can also be found in reactive lymphadenopathy (such as infectious mononucleosis immunoblasts which are RS like in appearance, carbamazepine associated lymphadenopathy) and very rarely in other types of non-Hodgkin lymphomas. Anaplastic large cell lymphoma may show RS like cells also…
https://en.wikipedia.org/wiki/Reed%E2%80%93Sternberg_cell

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Nicole Baumgarth, 2015, on B cell germinal center collapse (just as in Reed Sternberg, above) and the inability to then fight off viral infections:

Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection

 

PLOS

“Infections with the Lyme Disease agent, Borrelia burgdorferi, often fail to generate long-term protective immunity. We show here that this is because the immune system of the Borrelia-infected host generates only short-lived, structurally abnormal and non-functional germinal centers. These germinal centers fail to induce memory B cells and long-lived antibody-producing plasma cells, leaving the host susceptible to reinfection with Bb. This inability to induce long-term immunity was not due to the nature of Borrelia antigens, as even T-dependent antigens of Borrelia were unable to induce such responses. Moreover, influenza vaccine antigens, when applied during Borrelia-infection, failed to induce strong antibody responses and immune-protection from influenza challenge. This data illustrate the potent, if temporal, immune suppression induced by Borrelia-infection. Collectively, the data reveal a new mechanism by which Bburgdorferi subverts the adaptive immune response.”

http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1004976

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And now you see OspA or LYMErix does the same thing:  “Pam3Cys keeps the precursors on a more immature stage.”
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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 SNobrega A.

Author information

AbstractThe 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

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And this is Paul Duray publishing in IDSA’s journal in 1992:

170207_duray_1989

https://www.ncbi.nlm.nih.gov/pubmed/2814170

and
http://www.actionlyme.org/IDSA_CLINIPATH_DURAY.htm

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So, make sure whoever is selling you any Lyme voodoo treatments provides you with the scientific evidence that shows their treatment program reverses this condition with the published, reproduced, valid science.

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2 thoughts on “Steere and Pseudolymphoma from Lyme and LYMErix; “Reed-Sternberg Cells”

  1. Pingback: Status of Forces, End of 2017 | Cryme Disease - Unscrambling the CDC's DNA Patent Profiteering Bullshit

  2. Pingback: Why TruthCures and ActionLyme dont Rx treatments for tick bite sepsis…. | Cryme Disease - Unscrambling the CDC's DNA Patent Profiteering Bullshit

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