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The sum of the affinities for various host tissue
molecules, masking, and inhibition of complement
action are part of the picture of mechanisms of
persistence. In vitro studies with antibodies
("borreliacidal") inhibition do not show the entire
dynamic.
It is now known that B cells play an important role
in autoimmune disease. Somatic mutation and perhaps
inhibition of normal timed cell death. The result is
a component of "autoimmune" disease that should not
be ovelooked in favor of the second line of defense,
T cells.
Borrelia and Glycosphingolipids
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=PureSearch&db=PubMed&details_term=%28%28%22borrelia%22%5BMeSH%20Terms%5D%20OR%20borrelia%5BText%20Word%5D%29%20AND%20%28%22glycosphingolipids%22%5BMeSH%20Terms%5D%20OR%20glycosphingolipid%5BText%20Word%5D%29%29
Borrelia AND Ligand
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=PureSearch&db=PubMed&details_term=%28%28%22borrelia%22%5BMeSH%20Terms%5D%20OR%20borrelia%5BText%20Word%5D%29%20AND%20%28%22ligands%22%5BMeSH%20Terms%5D%20OR%20ligand%5BText%20Word%5D%29%29
Borrelia AND Decorin
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=PureSearch&db=PubMed&details_term=%28%28%22borrelia%22%5BMeSH%20Terms%5D%20OR%20borrelia%5BText%20Word%5D%29%20AND%20%28%22decorin%22%5BSubstance%20Name%5D%20OR%20decorin%5BText%20Word%5D%29%29
Borrelia AND Fibronectin
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=PureSearch&db=PubMed&details_term=%28%28%22borrelia%22%5BMeSH%20Terms%5D%20OR%20borrelia%5BText%20Word%5D%29%20AND%20%28%22fibronectins%22%5BMeSH%20Terms%5D%20OR%20fibronectin%5BText%20Word%5D%29%29
Borrelia AND Complement
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=PureSearch&db=PubMed&details_term=%28%28%22borrelia%22%5BMeSH%20Terms%5D%20OR%20borrelia%5BText%20Word%5D%29%20AND%20%28%22complement%22%5BMeSH%20Terms%5D%20OR%20complement%5BText%20Word%5D%29%29
Borrelia AND Lymphocyte binding
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=PureSearch&db=PubMed&details_term=%28%28%22borrelia%22%5BMeSH%20Terms%5D%20OR%20borrelia%5BText%20Word%5D%29%20AND%20%28%28%22lymphocytes%22%5BMeSH%20Terms%5D%20OR%20lymphocyte%5BText%20Word%5D%29%20AND%20%28%28%22pharmacokinetics%22%5BSubheading%5D%20OR%20%22pharmacokinetics%22%5BMeSH%20Terms%5D%29%20OR%20binding%5BText%20Word%5D%29%29%29
Borrelia and plasmin
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=PureSearch&db=PubMed&details_term=%28%28%22interleukin-6%22%5BMeSH%20Terms%5D%20OR%20IL-6%5BText%20Word%5D%29%20AND%20psychiatric%5BAll%20Fields%5D%29
Borrelia and OspA/P66 (Porins can be protected by Osps)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=PureSearch&db=PubMed&details_term=%28%28%28%22borrelia%22%5BMeSH%20Terms%5D%20OR%20Borrelia%5BText%20Word%5D%29%20AND%20OspA%5BAll%20Fields%5D%29%20AND%20P66%5BAll%20Fields%5D%29
Borrelia and Porin
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=PureSearch&db=PubMed&details_term=%28%28%22borrelia%22%5BMeSH%20Terms%5D%20OR%20Borrelia%5BText%20Word%5D%29%20AND%20%28%22porins%22%5BMeSH%20Terms%5D%20OR%20porin%5BText%20Word%5D%29%29
Rheumatoid Arthritis and B cells (RA as a probable B cell Lymphoma)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=PureSearch&db=PubMed&details_term=%28%28%28%22arthritis%2C%20rheumatoid%22%5BMeSH%20Terms%5D%20OR%20Rheumatoid%20arthritis%5BText%20Word%5D%29%20AND%20%28%22b-lymphocytes%22%5BMeSH%20Terms%5D%20OR%20B%20cell%5BText%20Word%5D%29%29%20AND%20%28%22mutation%22%5BMeSH%20Terms%5D%20OR%20mutation%5BText%20Word%5D%29%29
Noteworthy
Clonal expansion is a characteristic feature of the
B-cell repertoire of patients with rheumatoid arthritis
http://arthritis-research.com/content/2/1/50
Multiple Sclerosis and B cell mutation
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=PureSearch&db=PubMed&details_term=%28%28%28%22b-lymphocytes%22%5BMeSH%20Terms%5D%20OR%20B%20cell%5BText%20Word%5D%29%20AND%20%28%22mutation%22%5BMeSH%20Terms%5D%20OR%20mutation%5BText%20Word%5D%29%29%20AND%20%28%22multiple%20sclerosis%22%5BMeSH%20Terms%5D%20OR%20multiple%20sclerosis%5BText%20Word%5D%29%29
Somatic Mutation of the V:
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=pubmed_pubmed&from_uid=8282807
'nother freebie:
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11299060&dopt=Abstract
"Most of the rearranged genes were mutated
(range, 1-15%). Thirty of 70 products had a
mutational pattern typical for antigen selection."
Heavy chains/Variable/CNS diseases
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=PureSearch&db=PubMed&details_term=%28%28heavy%20chain%5BAll%20Fields%5D%20AND%20variable%5BAll%20Fields%5D%29%20AND%20%28%22central%20nervous%20system%20diseases%22%5BMeSH%20Terms%5D%20OR%20CNS%20disease%5BText%20Word%5D%29%29
'RESULTS: As expected for an antigen-driven response
against MV antigens, most VH sequences from the SSPE
brains were ***mutated extensively compared with their
closest germline segments***. Furthermore, SSPE VH
sequences accumulated replacement mutations preferentially
in the complementary-determining regions (CDRs) relative
to framework regions-features normally observed during
antigen-driven selection. A comparison of VH family
and germline usage also demonstrated that each SSPE brain
had its own unique IgG response. ***When the authors compared
the VH response in MS plaques with SSPE, MS VH sequences
were also mutated extensively, displayed a preferential
accumulation of replacement mutations in CDRs, and were
unique in each MS brain.
CONCLUSION: The presence of an antigen-driven response in
MS, rather than a nonconventional mechanism of B-cell
activation, warrants additional analysis of the specificity
of IgG in MS brain and CSF."
"PRESENCE OF AN ANTIGEN DRIVEN RESPONSE"
"SPECIFICITY of IgG in MS brain and CSF"
The multiple etiologies of Neuroautoimmune disorders
include exposure to Campylobacter, Helicobacter, HHVs,
Borrelia, Chlamydia, possibly HERVs, possibly prion
diseases. Chlamydia is an intracellular organism with
a spore-like stage, similar to Borrelial Spheroplast.
The Borrelial spheroplast doesn't typically stain.
Viral diseases of neurons may also show no histological
changes to neurons.
Physiological and psychological stress are
thought to upregulate heat shock proteins,
possibly making them targets of autoreactive
to bacterial heat shock protein antibodies.
Some infections result in CNS cell loss
due to presentation of Class I antigens by
CNS cells:
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=pubmed_pubmed&from_uid=11583948
===============
Molecular Midgetry:
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=PureSearch&db=PubMed&details_term=%28Steere%20AC%5BAuthor%20Name%5D%20AND%20%28%22t-lymphocytes%22%5BMeSH%20Terms%5D%20OR%20T%20cells%5BText%20Word%5D%29%29
page updated 7 November 2001
KMD