‘Not surprising since Treponemes are also shedders of TLR2/1 agonists (Radolf). Keep in mind, Baseman, also.
“Evidence is presented which reinforces the complexity of the host-parasite interaction during the course of syphilis. Infection with Treponema pallidum evokes a complicated antibody response and an assortment of cell-mediated immune reactions in the host. It appears that humoral immunity plays a minor role towards the complete elimination of syphilitic infection while the cellular limb of the immune response may be an important host defence mechanism. Information now available indicates that a state of anergy, or immunosuppression, exists in the early stages of human and experimental rabbit syphilis based upon negative skin reactions to T. pallidum antigen(s), the abnormal histological appearance of lymphoid organs, and impaired in vitro lymphocyte reactivity. It is also evident that in the later stages of the disease cellular immunity becomes activated as delayed type skin reactions can normally be elicited in tertiary syphilitics and lymphocyte behaviour in cell culture appears normal. Several mechanisms have been invoked to explain the delay in an effective immune response against syphilitic infection and the duration of the disease: (1) a capsule-like substance on the outer surface of virulant T. pallidum may act as a barrier against treponemicidal antibody; (2) this material and other biological properties of virulent treponemes could enable spirochaetes to escape being engulfed by macrophages and other phagocytic cells; (3) antigenic competition among different treponemal antigens causing partial tolerance; (4) T. pallidum infection may bring about the elaboration of immunosuppressive substances of host or treponemal origin which inhibit the proper function of lymphocytes, macrophages, and other cell types.”
Radolf saying spirochetes and mycobacteria/mycoplasma are bearers/shedders of fungal antigens (and also Brucella, Bart, Babs, et al) and cause immunosuppression. This report also demonstrates why it is important to know Spirochaeta are their own PHYLUM (means they are not evolutionarily related to anything else) and not plain old regular “bacteria.”
Toll-like Receptor 2 Functions as a Pattern Recognition Receptor for Diverse Bacterial Products*
“The cellular activation induced by the lipoproteins or lipoprotein-derived lipopeptides from B. burgdorferi andT. pallidum resembles that of the LPS signaling pathway, as CD14 appears to facilitate cellular activation by both types of pathogenic membrane structures (21, 25). However, several differences have been observed between LPS and lipoprotein cellular activation, indicating the utilization of different signaling elements. For example, spirochetal and mycoplasma lipoproteins and lipopeptides activate macrophages from LPS hyporesponsive C3H/HeJ mice (23, 24, 27,31). In addition, whereas Chinese hamster ovary (CHO)-K1 cells become remarkably sensitive to LPS after transfection with CD14 (34-36), they remain insensitive to the lipoproteins, lipopeptides, and motileB. burgdorferi (21, 30, 32). These observations led us to hypothesize that differences in main signaling components exist between lipoproteins and LPS.”
That one single ^^ report shows neither IDSA or ILADS, nor Yale, the CDC, NYU, Johns Hopkins or anyone else who claims to understand Lyme disease, really has any idea what they are talking about. Spirochetes are spirochetes (phylum) and shed fungal antigens that turn off the immune response and this was well-known since at least the 1970s.
And in this report I am showing you that it was well known that the first Great Imitator was ALSO a disorder of immunosuppression. That is, I am showing you more data in parallel that shows the mechanisms of disease here in this report on Syphilis also being an immune suppressor. See also the Occam’s Razor and the SASH Policy Paper on Autism vaccines, ME, CFS, Lyme etc, from 2015:
Baseman and Tully; J. G. Tully is a known bioweaponeer:
And this is in the CDC’s own journal:
Mycoplasmas: sophisticated, reemerging, and burdened by their notoriety.
“Mycoplasmas are most unusual self-replicating bacteria, possessing very small genomes, lacking cell wall components, requiring cholesterol for membrane function and growth, using UGA codon for tryptophan, passing through “bacterial-retaining” filters, and displaying genetic economy that requires a strict dependence on the host for nutrients and refuge. In addition, many of the mycoplasmas pathogenic for humans and animals possess extraordinary specialized tip organelles that mediate their intimate interaction with eucaryotic cells. This host-adapted survival is achieved through surface parasitism of target cells, acquisition of essential biosynthetic precursors, and in some cases, subsequent entry and survival intracellularly. Misconceptions concerning the role of mycoplasmas in disease pathogenesis can be directly attributed to their biological subtleties and to fundamental deficits in understanding their virulence capabilities. In this review, we highlight the biology and pathogenesis of these procaryotes and provide new evidence that may lead to increased appreciation of their role as human pathogens.”
Keep in mind that CDC officer Suzanne Vernon threw out the mycoplasma (which attach to cells especially red blood cells causing hypoxia, ie., fatigue) before allegedly not finding mycoplasma in Chronic Fatigue/ME patients.
You’ve just seen another in-parallel model of the disease we have been showing you that is caused by OspA alone, with or without spirochetes. It is called “Post Sepsis Syndrome” (even the CDC officially calls it this as does the NIH), Endotoxin Tolerance, T and B cell “anergy,” immunosenescence, acquired immune deficiency, CFIDS, ME/CFS, Chronic Lyme, Mitochondrial Disorder, Fibromyalgia, etc.