Post-Streptococcal Autoimmune Sequelae: A Link Between Infection and Autoimmunity

Kotb, Malak

doi:10.1007/978-94-011-1108-9_6

Cited by 2 publications

(2 citation statements)

References 46 publications

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“…Analysing this hypothesis, Demellawy et al, have shown that T cells from RHD patients exhibit increased reactivity to human myocardial antigens after priming of PBMC with rheumatogenic streptococci [34]. The same group demonstrated that the stimulation of T cells with pepsin extracted M5 protein (a major streptococcal antigen), enhances the ability of lymphocytes to recognize and respond to cardiac myosin [35]. Myosin is known to bear structural homology to M protein and is also an important target autoantigen in RHD [36].…”

Section: Discussionmentioning

confidence: 95%

Restriction in the Usage of Variable β Regions in T-cells Infiltrating Valvular Tissue from Rheumatic Heart Disease Patients

Figueroa

González

Carrión

et al. 2002

Journal of Autoimmunity

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Section: Discussionmentioning

confidence: 95%

Restriction in the Usage of Variable β Regions in T-cells Infiltrating Valvular Tissue from Rheumatic Heart Disease Patients

Figueroa

González

Carrión

et al. 2002

Journal of Autoimmunity

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“…Alternatively, the enhanced cellular recognition of myocardial antigens following stimulation with opsonized bacteria may be mediated by streptococcal superantigens, including M proteins (61), that stimulate T cells based on the V␤ type and regardless of the antigenic specificity of the T-cell receptor. It has been suggested that, through this mode of stimulation, superantigens can potentially activate autoreactive T cells (17,29,32,42,52,53). The latter possibility is supported by previous studies in our laboratory demonstrating that stimulation of T cells with pepsin-extracted M5 protein enhanced their ability to recognize and respond to cardiac myosin (29).…”

Section: Discussionmentioning

confidence: 55%

Preferential recognition of human myocardial antigens by T lymphocytes from rheumatic heart disease patients

et al. 1997

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Acute rheumatic fever (ARF) and rheumatic heart disease (RHD) are autoimmune sequelae of upper respiratory infections with group A streptococci (GAS). To gain a better understanding of the pathogenesis of these diseases, we examined the in vitro proliferative responses of peripheral blood mononuclear cells (PBMC) from RHD patients to human myocardial proteins in a T-cell Western assay. A number of myocardial proteins fractionated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis were recognized by PBMC from both patients and controls. However, PBMC from a significant percentage of RHD patients (40%) responded to a discrete band of myocardial proteins migrating with an apparent molecular mass of 50 to 54 kDa while none of the control subject PBMC responded to this protein band (P < 0.0001). To further investigate the link between infections with GAS and autoimmune carditis, we studied the proliferative responses of PBMC from patients and controls to myocardial proteins before and after in vitro stimulation of the cells with opsonized GAS isolated from ARF patients. Priming of PBMC with rheumatogenic GAS caused the percentage of RHD patients responding to the 50-to 54-kDa myocardial proteins to increase from 43 to 90% (P < 0.0284). By contrast, PBMC from control subjects failed to recognize the 50-to 54-kDa myocardial proteins even after stimulation with the opsonized streptococci (P < 0.0001). The assay sensitivity was increased from 40 to 90% after priming of a patient's cells with opsonized GAS, but the positive predictive value was 100% in both unprimed and primed cultures. Antibodies generated to partially purified 50-to 54-kDa myocardial proteins did not cross-react with either streptococcal homogenates, purified M protein, myosin, laminin, or vimentin, suggesting a lack of cross-reactivity at the humoral level. This study suggests that the 50-to 54-kDa myocardial proteins contain a putative antigen that is preferentially recognized by T cells from RHD patients and demonstrates that exposure to streptococcal antigens enhances the ability of patients to recognize these proteins.

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Post-Streptococcal Autoimmune Sequelae: A Link Between Infection and Autoimmunity

Cited by 2 publications

References 46 publications

Restriction in the Usage of Variable β Regions in T-cells Infiltrating Valvular Tissue from Rheumatic Heart Disease Patients

Restriction in the Usage of Variable β Regions in T-cells Infiltrating Valvular Tissue from Rheumatic Heart Disease Patients

Preferential recognition of human myocardial antigens by T lymphocytes from rheumatic heart disease patients

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