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Re: CVID/Immune Deficiencies, TNF Gene Mutations, and Lyme

Posted: Wed 12 Aug 2015 16:20
by X-member
I have asked Swedish immunologists about borreliosis and my immune deficiency (I have both low total IgG and low total IgA) but they don't know how it is when it comes to borreliosis, but you hv808ct know (or think?) that an immune deficiency (like mine) is "no problem"?

Re: CVID/Immune Deficiencies, TNF Gene Mutations, and Lyme

Posted: Sun 16 Aug 2015 1:51
by X-member
Maybe this belong in this thread?

Our experience with examination of antibodies against antigens of Borrelia burgdorferi in patients with suspected lyme disease.

http://www.ncbi.nlm.nih.gov/pubmed/20437826

A quote:
CONCLUSION:
In patients with persisting difficulties that could be associated with Lyme disease, it is necessary to use the westernblot test which could prove the presence of specific antibodies. It is probably due to the very low production of specific antibodies caused also by the status of immune deficiency detected in all our patients (Tab. 1, Ref. 11).

Re: CVID/Immune Deficiencies, TNF Gene Mutations, and Lyme

Posted: Sun 16 Aug 2015 2:00
by ChronicLyme19
Oh, good find! That looks like a good one. I want to see if I can get the full text.
All patients had specific antiborrelial antibodies confirmed by using the westernblot in spite of negative ELISA. Immunological investigations revealed a deficiency of cellular immunity in all patients and in a part of them (15.6%) a deficiency of humoral immunity was also found. The presence of different types of autoantibodies was detected in 17 (53.1%) patients.

Re: CVID/Immune Deficiencies, TNF Gene Mutations, and Lyme

Posted: Mon 17 Aug 2015 6:53
by dlf
This is another early study that previously has been posted elsewhere on the forum, but this seems like a good place to re-introduce it. Full text and really interesting photos.....

http://cid.oxfordjournals.org/content/2 ... _1/S2.long
Clin Infect Dis. 1997 Jul;25 Suppl 1:S2-8.
Invasion and cytopathic killing of human lymphocytes by spirochetes causing Lyme disease.
Dorward DW1, Fischer ER, Brooks DM.
1National Institute of Allergy and Infectious Diseases, Rocky Mountain Laboratories, Hamilton, Montana 59840, USA.
Abstract
Lyme disease is a persistent low-density spirochetosis caused by Borrelia burgdorferi sensu lato. Although spirochetes causing Lyme disease are highly immunogenic in experimental models, the onset of specific antibody responses to infection is often delayed or undetectable in some patients. The properties and mechanisms mediating such immune avoidance remain obscure. To examine the nature and consequences of interactions between Lyme disease spirochetes and immune effector cells, we coincubated B. burgdorferi with primary and cultured human leukocytes. We found that B. burgdorferi actively attaches to, invades, and kills human B and T lymphocytes. Significant killing began within 1 hour of mixing. Cytopathic effects varied with respect to host cell lineage and the species, viability, and degree of attenuation of the spirochetes. Both spirochetal virulence and lymphocytic susceptibility could be phenotypically selected, thus indicating that both bacterial and host cell factors contribute to such interactions. These results suggest that invasion and lysis of lymphocytes may constitute previously unrecognized factors in Lyme disease and bacterial pathogenesis.

Re: CVID/Immune Deficiencies, TNF Gene Mutations, and Lyme

Posted: Mon 17 Aug 2015 16:21
by ChronicLyme19
Differences in killing of lymphocytes by different species of Borrelia were noted in this study. Although both the B. hermsii isolate (tick-borne relapsing fever agent) and the B. afzelii isolate (Lyme borreliosis agent) that were used were infectious in mice [23], neither isolate caused an increase in the number of killed SKW 6.4 cells. B. hermsii, like other relapsing fever agents, can repeatedly reach levels of 10^6–7 per milliliter of peripheral blood in patients [27]. At those levels, if lymphocytes were susceptible to killing by spirochetes causing relapsing fever, severe immune deficiencies in patients could be expected. Such consequences are inconsistent with typical clinical manifestations. We also found differences in killing of lymphocytes by Lyme disease spirochetes. Further investigation with use of additional isolates should elucidate whether such differences correlate with observed predilections of B. afzelii for dermatologic manifestations and of B. burgdorferi and B. garinii for disseminated disease [28].
Maybe if you get multiple species of borrelia and co-infections it would be quiet enough to take down your immune system and cause the IgM/IgG/IgA deficiencies we see in a subset of chronic lymees.
Humoral immunity is protective in laboratory animals [29]; in contrast, humoral responses are typically delayed in patients. In vitro spirochete-leukocyte interactions may provide an effective model for understanding the delayed immune response in humans when they are infected by Lyme disease spirochetes.
I wonder if this helps explain the weird Ig Response Pattern #2 (see image at top of thread).

Re: CVID/Immune Deficiencies, TNF Gene Mutations, and Lyme

Posted: Tue 2 Feb 2016 5:05
by ChronicLyme19
Thought this might belong in this thread for what it's worth. I recently moved states and went to a new immunologist. New immunologist noted he had several people who had an onset of CVID concurrent with the onset of chronic Lyme and based on his medical review of their cases they did not have CVID pre-Lyme. I know this doesn't necessarily imply causation, but this is the first immunologist I have talked to that believes there is a type of CVID that is Lyme induced.

Re: CVID/Immune Deficiencies, TNF Gene Mutations, and Lyme

Posted: Sat 19 Nov 2016 14:31
by ChronicLyme19
This is crossing threads a bit, but I am now coming across a few people in the immune support groups who have hypogammaglobulinemia and MS. And I know many of us on here have had the discussion before about there being no distinguishing feature between MS and late stage Lyme. This would match with the two theories 1) some MS cases are actually misdiagnosed late stage Lyme cases 2) some cases of late stage Lyme can cause immune deficiencies like hypogammaglobulinemia (also leading them to repeatedly negative for Lyme). So it make sense that if some MS cases are actually late stage borrelia infections, and if borrelia species could cause hypogammaglobulinemia, that we would see MS patients getting diagnosed with hypogammaglobulinemia.

http://www.jacionline.org/article/S0091 ... 0/abstract