Ok, so I went through and tried to summarize the one article by some of the same authors. Dlf, you were right, it said B.b highly favors IgM production and the IgGs never really get produced well. This adds to the reasons why the test miss half the cases. If you miss the small window where you do get some IgG response, you won't test positive.
Delays and Diversions Mark the Development of B Cell Responses to Borrelia burgdorferi Infection
Christine J. Hastey, Rebecca A. Elsner, Stephen W. Barthold and Nicole Baumgarth
http://www.jimmunol.org/content/188/11/5612.long
Published online before printApril 30, 2012, doi: 10.4049/jimmunol.1103735
The Journal of Immunology June 1, 2012 vol. 188 no. 11 5612-5622
Conclusions
-“Alters normal B cell response development in the lymph nodes in multiple ways”, suggesting “that B. burgdorferi-infected mice might be unable to develop strong T-dependent germinal centers and thereby might lack long-lived plasma cells and memory responses.”
-Dominated by “Unusually strong and persistent T-dependent and T-independent IgM Abs”, “both induced early in the lymph nodes and also found later in the bone marrow”, a good fraction of which is T-dependant. Most likely a result of a non-class-switched B-2 cell response and not likely T-independent B-1 cells (blood) or B-2 cells (bone marrow).
-“Because of its large size, IgM might not be able to reach B. burgdorferi in the tissues in the absence of inflammation and the resulting increase in vascular leakage” and therefore is harder to clear the infection from tissues.
-“The data thereby suggest that B. burgdorferi might interfere with the processes underlying efficient class-switch recombination of B cells.”
-“They failed to mount strong T-dependent B cell responses and formed only transient germinal centers.“
-“The destruction of the lymph node architecture”
-“B cells rapidly and strongly accumulate in regional lymph nodes in response to the presence of live B. burgdorferi, but independent of either MyD88 signaling (5) or T cell help”.
-“Given the fact that passive transfer of serum Abs from mice infected for 2 mo can protect from challenge with B. burgdorferi (15), the same serum is unable to clear an infected host” and serum from long-term infected mice loses this capacity“. “Even relatively minor delays in induction of protective Ab responses might play a role in allowing B. burgdorferi to evade immunity by rapidly and widely disseminating in an infected host (35).”
-“Ongoing dynamic interaction between the host adaptive immune system and the spirochetes in long-term B. burgdorferi-infected hosts that ultimately benefits the spirochete, enabling establishment of persistent infections.”
Immune Response Stages
1) “The initial phase is dominated by a strong T-independent accumulation of B cells in lymph nodes and the induction of specific Abs in the absence of germinal centers.”
3) “A second phase begins around week 2.5 to 3, in which relatively short-lived germinal centers develop in lymph nodes, despite a lymph node architecture that lacks clearly demarcated T and B cell zones. This response failed, however, to generate appreciable numbers of long-lived bone marrow plasma cells. “
3) “Finally, there is a slow accumulation of long-lived Ab-secreting plasma cells in bone marrow, reflected by a strong, but ultimately ineffective serum Ab response.”
B. burgdorferi & B cells
-“B cell responses modulate” & “control of disease progression and resolution”... “but are unable to clear the infection.”
-“In wild-type mice, as B cell deficiency resulted in more severe disease”
-“Support for a role of B. burgdorferi-specific Abs in B cell-mediated disease resolution comes from studies showing that passive transfer of serum from infected, but not naive, immune-competent mice results in arthritis and carditis resolution in SCID mice “
-“Given the fact that passive transfer of serum Abs from mice infected for 2 mo can protect from challenge with B. burgdorferi (15), the same serum is unable to clear an infected host” and serum from long-term infected mice loses this capacity“.
-“predominantly T-independent B cell responses”
-“increased lymph node cellularity shortly postinfection was attributable in large part to the accumulation of CD19+ B cells”
-“the ratio of CD19+ B cells to CD4+ T cells increased in the lymph nodes, with increasing numbers of B cells per CD4 T cell at early time points, peaking at day 10. That ratio stayed elevated through day 60.”
-Total B cell counts were normal, increase in frequency was localized and T cell independent.
B. burgdorferi & T cells
-Others have shown T cells & CD40L modulate the isotype profile and “amplify and regulate the quality of the B. burgdorferi-specific Ab response.”
-“CD4 T cells engage with B cells in a CD40L- and SAP-dependent but ICOS-independent manner to enhance early B. burgdorferi-specific Ab responses in lymph nodes”
-“T cell deficiency had little impact on arthritis resolution and the development of other inflammatory disease manifestations.”
-Adding T cells made inflammation worse.
-“Overall T cell numbers do not significantly increase in lymph nodes”
-“The unusually high B/T ratio might suggest that CD4 T cells were not activated upon infection”, however “transient and short-lived CD4 T cell activation and differentiation to TFH nonetheless occurred.”
-“The kinetics of germinal center B cells closely followed that of the TFH cell population (Fig. 2A), appearing somewhat slow in induction and very rapid in decline”, “between days 21 and 28.”
-“Depletion of CD4 T cells caused a significant reduction in germinal center B cells, as did the absence of CD40L−/− and SAP−/− mice”
Half of what you are taught is incorrect, but which half? What if there's another half missing?
