LymeNet Europe

Posted: **Thu 3 Mar 2016 4:05**

LHCTom wrote:The subclass deficiency would contribute to less effective spirochete ( or bacterial and viral in general) killing off. If both the innate/cellular immune system is blunted and infectious Ab production lowered, that may be an aquired form of immune suppresion that inhibits the killing off of the last viral or bacterial cell enabling persistence. Throw in a few spirochete persisters and we are off to the races - over and over and over.... Is correcting the Th1/Th2 balance part of the problem? Plus correcting the IgG1/3 deficiency? Just a crazy thought.

That could maybe help explain why my immunologist says half of his CVID patients have chronic Lyme infections. Lyme is very common, so it would just be a matter of time before those with CVID or other PIDs would run into it and get stuck.

Now only if someone could prove whether or not Lyme also causes Ig deficiencies, so we'd know if it was the chicken or the egg that started it. Or perhaps one of the other tick borne infections triggers the deficiencies, which gives Lyme the foothold...

One of my biggest beefs with the IDSA guidelines is that they do not consult the immunology community. I wish the clinical immunologists would pair up with the infectious disease docs and put their heads together.

Posted: **Sun 13 Mar 2016 17:57**

Some major assumptions....

Immunologic reaction to infection with B. burgdorferi includes a robust Ab response to a number of the organism’s proteins and glycolipids.

VlsE elicits a rapid and strong humoral response that can be detected throughout the course of the disease (18–20)

All patients met the U.S. Centers for Disease Control and Prevention case definition for Lyme disease (25). Patients with EM had culture evidence of B. burgdorferi infection. Early neurologic Lyme disease was defined as the presence of compatible objective clinical findings (e.g., cranial nerve palsy, lymphocytic meningitis, and/or radiculoneuritis) in conjunction with current or recent EM and/or serologic evidence of the infection. Late neurologic Lyme disease was defined based on the presence of a compatible objective clinical finding (e.g., encephalopathy, polyneuropathy, or encephalomyelitis) in association with serologic evidence of borrelial infection. Lyme arthritis was defined as the presence of clinically compatible joint swelling in conjunction with serologic evidence of the infection.

What serological evidence was enough to be included? Wouldn't you want to include those with weak immune response since they would have a much harder time fighting off the infection?

For immunoassays, biotin-labeled peptides representing the sequences of the three major epitopes of the VlsE protein of B. burgdorferi B31 (21, 24) were synthesized by using Fmoc chemistry (Sigma-Aldrich)

No others beside B31? Ah, it seems they do touch upon this limitation in the discussion section.

This study focused on the IgG Ab response because our initial data indicated minimal IgM response in patients against VlsE, which is consistent with the findings of prior studies (22).

It would have been nice to include IgM as well.

However, the described epitopes were found to be inaccessible to Abs on intact spirochetes.

Interesting.

LymeNet Europe

Evolution of Human B Cell Responses to Bb VlsE Protein from Early to Late Stages of Lyme Disease

Re: Evolution of Human B Cell Responses to Bb VlsE Protein from Early to Late Stages of Lyme Disease

Re: Evolution of Human B Cell Responses to Bb VlsE Protein from Early to Late Stages of Lyme Disease