Overlapping humoral autoimmunity links rheumatic fever and the antiphospholipid syndrome

Blank, Miri; Krause, Ilan; Magrini, L.; Spina, Guilherme Sobreira; Kalil, Jorge; Jacobsen, Søren; Thiesen, Hans‐Jürgen; Cunningham, Madeleine W.; Guilherme, Luiza; Shoenfeld, Yehuda

doi:10.1093/rheumatology/kel118

Cited by 39 publications

(32 citation statements)

References 60 publications

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“…These patients develop autoantibodies to b-2-glycoprotein-I (b2GPI), which may be induced by molecular mimicry [6,163]. In a subset of patients with APS and chorea, serum reacted with streptococcal GlcNAc, and the interaction was inhibited with b2GPI, suggesting molecular mimicry between two antigens [164].…”

Section: Chronic Neuroborreliosismentioning

confidence: 99%

Molecular mimicry in neurological disease: what is the evidence?

Lee

Levin

2008

Cell. Mol. Life Sci.

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Autoimmune diseases are a leading cause of disability and are increasing in incidence in industrialized countries. How people develop autoimmune diseases is not completely understood, but is related to an interaction between genetic background, environmental agents, autoantigens and the immune response. Molecular mimicry continues to be an important hypothesis that explains how an infection with an environmental agent results in autoimmune disease of the nervous system and other target organs. Although molecular mimicry has yet to be unequivocally proven, in the past several years there has been a sharpening of its definition with better experimental data implicating it as a cause of neurological disease in humans.

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Section: Chronic Neuroborreliosismentioning

confidence: 99%

Molecular mimicry in neurological disease: what is the evidence?

Lee

Levin

2008

Cell. Mol. Life Sci.

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“…This situation can be interpreted as two or more rare diseases that are simultaneously present or the same disease displaying characteristics that belong to another disease. It is believed that similar immunological mechanisms between different autoimmune diseases can cross-over and display similar manifestations in a particular Up to 24% of patients with rheumatic fever can have ß2 glycoprotein-1 antibodies, which are characteristic of APS and, conversely, around 14% of patients with APS have anti-streptococcal M-protein antibodies, which are typical of rheumatic fever 1,9 . It is suggested that streptococcal infection may be a trigger for the production of anticardiolipin antibodies, which would help clarify the association between APS, SLE and rheumatic fever 9,10 .…”

Section: Discussionmentioning

confidence: 99%

“…However, little is known about the association between several autoimmune diseases. The present describes the assumption that the same immune mechanism would be responsible for distinct clinical manifestations, albeit with no pathophysiological proof of the phenomenon, particularly due to the rarity of cases 1 .…”

Section: Introductionmentioning

confidence: 87%

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Associação entre doenças imunológicas e suas manifestações clínicas semelhantes

Soeiro¹,

Almeida²,

Accorsi³

et al. 2012

Arq. Bras. Cardiol.

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“…Valvular E. W. Camargo · P. V. Freire · N. R. d. Santos School of Medicine, Santo Amaro University, São Paulo, SP, Brazil involvement occurs in both diseases and includes noninfectious verrucous vegetations, thickening of the valves, signiWcant valvular dysfunction, either insuYciency and/or stenosis [5].…”

Section: Introductionmentioning

confidence: 99%

Antiphospholipid syndrome plus rheumatic fever: a higher risk factor for stroke?

et al. 2011

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To compare clinical and laboratory findings between patients with primary antiphospholipid syndrome (PAPS) versus secondary APS due to rheumatic fever (APS-RF) (according to Jones criteria). Seventy-three APS patients (Sapporo criteria) were enrolled, and demographic, clinical, and laboratory data were collected. Exclusion criteria were heart congenital abnormalities and previous infectious endocarditis. Patients were divided into two groups: PAPS (n = 68) and APS-RF (n = 5). The mean current age, disease duration, frequencies of female gender, and Caucasian race were similar in APS-RF and PAPS patients (P > 0.05). Remarkably, the frequency of stroke was significantly higher in APS-RF compared to PAPS patients (80% vs. 25%, P = 0.02). Of note, echocardiogram of these patients did not show intracardiac thrombus. No significant differences were found in peripheral thromboembolic events (P = 1.0), pulmonary thromboembolism (P = 1.0), miscarriage (P = 0.16), thrombocytopenia (P = 0.36), arterial events (P = 0.58), and thrombosis of small vessels (P = 1.0). There were no differences in the frequencies of comorbidities such as diabetes mellitus, hypertension, smoking, and hyperlipidemia in both groups (P > 0.05). The frequencies of lupus anticoagulant, IgG, and IgM anticardiolipin were similar in two groups. APS patients associated with rheumatic fever without infective endocarditis may imply a high stroke risk as compared with PAPS, and future studies are needed to confirm this finding.

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Overlapping humoral autoimmunity links rheumatic fever and the antiphospholipid syndrome

Abstract: The results of our study, showing a considerable overlap of humoral immunity in RF and APS, support a hypothesis that common pathogenic mechanisms underlie the development of cardiac valve lesions and Central Nervous System abnormalities in both diseases.

Cited by 39 publications

References 60 publications

Molecular mimicry in neurological disease: what is the evidence?

Molecular mimicry in neurological disease: what is the evidence?

Associação entre doenças imunológicas e suas manifestações clínicas semelhantes

Antiphospholipid syndrome plus rheumatic fever: a higher risk factor for stroke?

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