iii FEBRE REUMÁTICA
iii FEBRE REUMÁTICA
iii FEBRE REUMÁTICA
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GUILHERME L<br />
e cols.<br />
Etiopatogenia da<br />
febre reumática<br />
REFERÊNCIAS<br />
PATHOGENESIS OF RHEUMATIC FEVER<br />
AND RHEUMATIC HEART DISEASE<br />
LUIZA GUILHERME, KELLEN C. FAÉ, JORGE KALIL<br />
1. Baggenstoss AH, Titus JL. Rheumatic and collagen<br />
disorders of the heart. In: Gould SE, ed. Pathology<br />
of the heart and blood vessels. 3 rd ed. Springfield,<br />
Illinois: Charles C. Thomas Publisher; 1968. p. 649-<br />
722.<br />
2. Fischetti VA. Streptococcal M protein. Sci Am.<br />
1991;264(6):58-65.<br />
3. DiSciascio G, Taranta A. Rheumatic fever in children.<br />
Am Heart J. 1980;99:635-58.<br />
4. Clarke CA, McConnell RB, Sheppard PM. ABO blood<br />
groups and secretor character in rheumatic carditis.<br />
Br Med J. 1960;1:21-3.<br />
5. Falk JA, Fleischman JL, Zabrieski JB, Falk RE. A<br />
study of HL-A antigen phenotype in rheumatic fever<br />
and rheumatic heart disease. Tissue Antigen.<br />
Rheumatic fever occurs as a delayed sequel of throat infection by Streptococcus<br />
pyogenes, affecting 3-4% of untreated children. Genetic susceptibility is associated<br />
with HLA class II alleles. Rheumatic fever patients presented an exacerbated humoral<br />
and cellular response against streptococci antigens that by similarities between<br />
the bacteria and host antigens, leads to heart tissue injury by a mechanism called<br />
molecular mimicry. The mitral and aortic valves are the tissue most affected. Our<br />
group has described by the first time the immunodominant segment of streptococci<br />
M5 protein (81-96 amino acid residues) and some heart tissue derived proteins that<br />
are simultaneously recognized by peripheral T cells and heart infiltrating T cell clones<br />
by molecular mimicry, mainly by HLA DR7 and DR53 rheumatic fever/rheumatic<br />
heart disease patients. Mononuclear cells that infiltrated the heart lesions produced<br />
essentially inflammatory cytokines (INFγ and TNFα). Interestingly, mononuclear cells<br />
from the valvular lesions presented scarce numbers of IL-4 positive cells, suggesting<br />
that the most severe lesions present in the valves are due to low numbers of<br />
cells producing the regulatory IL-4 cytokine. In conclusion, all the knowledge acquired<br />
in the pathogenesis of rheumatic fever/rheumatic heart disease defines rheumatic<br />
fever/rheumatic heart disease as a post-infection auto-immune disease mediated<br />
by cross reactive T cells and inflammatory cytokines.<br />
Key words: rheumatic fever, rheumatic heart disease, molecular mimicry, T lymphocytes,<br />
cytokines.<br />
(Rev Soc Cardiol Estado de São Paulo. 2005;1:7-17)<br />
RSCESP (72594)-1502<br />
1973;3:173-8.<br />
6. Ayoub EM, Barrett DJ, MacLaren NK, Krischer JP.<br />
Association of class II histocompatibility leukocyte<br />
antigens with rheumatic fever. J Clin Invest.<br />
1986;77:2019-26.<br />
7. Anastasiou-Nana M, Anderson JL, Carlquist JF, Nanas<br />
JN. HLA-DR typing and lymphocyte subset evaluation<br />
in rheumatic fever and rheumatic heart disease:<br />
a search for immune response factors. Am Heart<br />
J. 1986;112:992-7.<br />
8. Rajapakse CN, Halim K, Al-Orainey I, Al-Nozha M,<br />
Al-Aska AK. A genetic marker for rheumatic heart<br />
disease. Br Heart J. 1987;58(6):659-62.<br />
9. Bhat MS, Wani BA, Koul PA, Bisati SD, Khan MA,<br />
Shah SU. HLA antigen pattern of Kashmiri patients<br />
with rheumatic heart disease. Indian J Med Res.<br />
1997;105:271-4.<br />
Rev Soc Cardiol Estado de São Paulo — Vol 15 — N o 1 — Janeiro/Fevereiro de 2005 15
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