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Expert
Reviews in Molecular Medicine: http://www.expertreviews.org/
Accession information: Vol. 7; Issue 28; 9 December 2005 Abstract
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Major events triggering rheumatic heart disease lesions
Luiza Guilherme, Kellen Faé, Sandra E. Oshiro and Jorge Kalil
Figure 2. Major events triggering rheumatic heart disease lesions. (a) Infection of the throat with Streptococcus pyogenes results in presentation of streptococcal antigens by antigen-presenting cells such as macrophages, and priming of B cells and CD4+ T cells to produce a humoral and cell-mediated response against streptoccal antigens. (b) Some antibodies are capable of cross-recognition of heart proteins, facilitating cellular infiltration of CD4+ T cells recognising heart-tissue proteins by molecular mimicry, triggering heart lesions (Ref. 12). (c) In the valvular tissue, the deposition of crossreactive antibodies increases the expression of VCAM-1, which interacts with VLA-4 expressed on the surface of T cells and facilitates cellular infiltration (Refs 59, 60). Inflammatory cytokines such as TNF-a and IFN-g mediate the development of the lesions, and the low numbers of IL-4-producing cells contribute to the progression and maintenance of valvular lesions (Ref. 94). Abbreviations: IFN-g, interferon g; IL-4, interleukin 4; MHC, major histocompatibility complex; TCR, T-cell receptor; TNF-a, tumour necrosis factor a; VCAM-1, vascular cell adhesion molecule 1; VLA-4, very late antigen 4.
| References cited
in Figure 2
12 Guilherme, L. et al. (1995) Human heart-infiltrating T-cell clones from rheumatic heart disease patients recognize both streptococcal and cardiac proteins. Circulation 92, 415-420, PubMed 59 Galvin, J.E. et al. (2000) Cytotoxic mAb from rheumatic carditis recognizes heart valves and laminin. J Clin Invest 106, 217-224, PubMed 60 Roberts, S. et al. (2001) Pathogenic mechanisms in rheumatic carditis: focus on valvular endothelium. J Infect Dis 183, 507-511, PubMed 94 Guilherme, L. et al. (2004) Rheumatic heart disease: proinflammatory cytokines play a role in the progression and maintenance of valvular lesions. Am J Pathol 165, 1583-1591, PubMed |
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