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Papers of the Month - July 1998
My apologies, but I have gotten a bit behind with the Papers of
the Month feature. Our Department had its RRC site visit in July;
I took some time off in August; and it has been very busy since
Labor Day. Accordingly, I am going to take a couple of shortcuts
to get caught up...
Last spring an MGH CPC in New England Journal of Medicine was
*very* interesting, at least to me. The patient had a luetic
aortitis, with some of the same histological features of an
autoimmune response that we have observed in the typical AAA. So
I wrote a Letter to the Editor on the similarities, in hopes that
it might be published there. Sadly, but not unexpectedly, it was
rejected. Accordingly, I am going to put it up here; so that it
may finally find a resting place.
April 11, 1998
FROM: M. David Tilson, MD
Professor of Surgery
Columbia University and St. Luke's/Roosevelt Hosp
1000 Tenth Avenue
New York, NY 10583
phone 212-523-7780
fax 212-523-6495
mdt1@columbia.edu
Word Count - 252
LETTERS TO THE EDITOR:
New England Journal of Medicine
10 Shattuck Street
Boston, MA 02115
Case 10-1998 of the Case Records of the Massachusetts
General Hospital featured syphlitic aortitis with coronary ostial
stenosis. Figure 2 of the aortic histopathology demonstrated an
adventitial infiltrate of lymphocytes and plasma cells with
Russell bodies. The Russell bodies were not subject to
additional discussion.
Russell bodies are aggregates of immunoglobulin that are
hallmarks of autoimmune diseases and have been described as a
feature of the aortitis associated with the common abdominal
aortic aneurysm (AAA). Immunoglobulin G (IgG) purified from
specimens of AAA tissue is immunoreactive with adventitial matrix
fibrils of the aorta and with a protein of approximately 40 kDa
which we have called Aortic Aneurysm-Associated Protein 40 kDa
(AAAP-40). The cDNA's for additional aorta-specific antigenic
proteins have been cloned, which we called Kappafibs 1 and 2 in a
recent communication.
We have proposed a novel hypothesis for the pathogenicity of
Treponema pallidum (T pal) for the aorta, based on the notion of
molecular mimicry. If the amino acid sequence of a protein of
a microorganism has sufficient similarity to a self protein,
infection may initiate an autoimmune response resulting in
disease. Similarity of the T pal protein TPF1 (PID g136052) to
Kappafib-1 was evaluated by a pairwise alignment program (AllAll)
and displayed by LalnView,
both of which are available on the internet at the
Biologist's Control Panel of the Human Genome Project of the
Baylor College of Medicine. The shading scale above the
representations of the two sequences is the key to the degree of
similarity. Further work will be needed to identify which, if
any, of the numerous similarities may be a shared epitope.
REFERENCES
