research about HLA-DR impacts lyme

Nobody?

Exactly. And this could be a reason, why they are negative. Do you have a HLA gene test? What was the result?

http://www.columbia-lyme.org/patients/ld_chronic.html

still trying to digest this article

In conclusion, this study offers further evidence for the existence of an immune-related disease process in patients with persistent symptoms following antibiotic treatment for Lyme disease. It is the first report to demonstrate increased IFNα activity in affected patients, suggesting a potential mechanism contributing to the associated ongoing neuropsychiatric symptoms. In addition, there is a significantly enhanced antibody response to autoantigens and to specific borrelial proteins, possibly indicating prolonged exposure to the organism prior to the original diagnosis and treatment of Lyme disease The data also show that additional β-lactam antibiotic therapy is not effective at modulating the activated immune response in affected patients. The study's findings point to the possibility of discovering biomarkers that could help in identification of specific subsets of patients with, or at risk for developing, persistent symptoms. In addition, they yield novel clues regarding disease mechanism that may become useful in finding safe and effective treatments for affected individuals in the future.


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3557545/

found this interesting. Check out Figure 7. Are those IFIs genes?

Post Edited (Roxie60) : 10/9/2014 10:17:53 PM (GMT-6)

se.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3470953/

Why is this particular gene so important? The DR allele is responsible for presenting the antigen to the T cells for an immune system response. When the antigen is presented to the T cell in the context of the DR4 allele, T cells are stimulated to produce interferon gamma, an inflammatory response. In contrast, when the antigen is presented in the context of the DR11 allele, it stimulates the production of antibodies, a response that does not induce inflammation. The antibodies bind to the bacteria and eliminate it. So somehow the presence of either the DR4 or DR11 allele determines the T cell response — whether to produce interferon gamma and launch an inflammatory attack or to produce antibodies to the antigen, instead [25]. In the case of DR4, once the immune response has begun, it is self-perpetuating because interferon gamma will stimulate T cells to produce more interferon gamma. Thus the initial immune response determines the outcome of the disease in the long run.

act

The immunoglobulin G (IgG) antibody response to outer surface protein A (OspA) of Borrelia burgdorferi has been reported to occur late in the course of Lyme disease. To learn when reactivity to particular epitopes of OspA develops and whether the strength of particular responses correlates with the duration of arthritis and HLA-DR specificities, we determined the IgM and IgG responses by enzyme-linked immunosorbent assay in 128 patients with various manifestations of Lyme disease to full-length recombinant OspA and three OspA fragments which divided the protein approximately into thirds. Among the 10 patients who were followed serially, an early IgM response was often found to epitopes in all three fragments of OspA, sometimes accompanied by a weak IgG response, primarily to an epitope in the middle third of the protein. Months to years later, the seven patients who had prolonged or moderate episodes of arthritis developed strong IgG responses to OspA, especially to epitopes in the N-terminal and C-terminal fragments, that paralleled the course of the arthritis. In single serum samples from 128 patients, a similar pattern of IgM and IgG reactivity with OspA epitopes was seen in patients with early or late manifestations of the illness. Of the 80 patients with arthritis, 62 (78%) had IgG responses to OspA, usually with the strongest reactivity to the C-terminal fragment. In these patients, the strength of the IgG response to OspA correlated with the duration of arthritis; in HLA-DR4-positive patients, most of whom had chronic arthritis, this association was attributable to reactivity with the C-terminal fragment. Thus, patients with Lyme disease often have early responses to OspA, but those with prolonged arthritis do not develop IgG responses to certain epitopes of the protein until late in the illness. In patients with HLA-DR4, the strength of IgG reactivity with one or more epitopes in the C-terminal fragment of OspA correlates with the duration of arthritis.


http://www.ncbi.nlm.nih.gov/pubmed/7768602

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3749008/

http://www.survivingmold.com/diagnosis/lab-tests

very I teresting chart. Lists dr genes as relate to many issues lymies have

Apparently my lab was testing for DQ2 and DQ8 which supposedly indicate risk for Celiac. I have study genes a lot but I am struggling to understand these HLA genes. It appears there has to be a combination of genes that make up an HLA gene. As example, which is confusing to me for now, here is how my lab result indicated DQ2 and DQ8:

DQ2 (DQA1 0501/0505, DQB1 02XX) Negative
DQ8 (DQA1 03XX, DQB1 0302) Negative

Final Results:
DQA1*03:MN.06:01
DQB1*03:XMSJ,03:XMSK

If I could figure out the code I would try to investigate DR4 and DR2 as it relates to antibody suppression and arthritis in lyme patients

HLA DR4 DRB1*04:01 is associated with multiple sclerosis,[12] rheumatoid arthritis,[13] type 1 diabetes,[14][15] lyme disease induced arthritis[16]

this is from HLA DR4 wiki

What a rabbit hole thiis is, my brain hurts. And no further trying to figure out how my HLA genes might impact the efficacy of using antibiotics.