Antiphospholipid syndrome associated with infections: clinical and microbiological characteristics

Cervera, Ricard; Asherson, Ronald A.

doi:10.1016/j.imbio.2005.10.003

Cited by 45 publications

(34 citation statements)

References 57 publications

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“…While both associations with certain HLA types and reactivity against the self-protein vimentin are in line with the concept of autoimmunity, a seasonal distribution of disease onset [30], as well as the fact that sarcoidosis (especially Löfgren's syndrome) normally runs a self-limiting disease course, would argue against. Moreover, there are examples of transient autoimmunity following infection [38,39], consistent with our previous finding that strong anti-vimentin T-cell responses were absent in patients after recovery [33].…”

Section: Vβ22supporting

confidence: 91%

T-cell receptor–HLA-DRB1 associations suggest specific antigens in pulmonary sarcoidosis

et al. 2015

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In pulmonary sarcoidosis, CD4+ T-cells expressing T-cell receptor Vα2.3 accumulate in the lungs of HLA-DRB1*03 + patients. To investigate T-cell receptor-HLA-DRB1*03 interactions underlying recognition of hitherto unknown antigens, we performed detailed analyses of T-cell receptor expression on bronchoalveolar lavage fluid CD4 + T-cells from sarcoidosis patients. Pulmonary sarcoidosis patients (n=43) underwent bronchoscopy with bronchoalveolar lavage. T-cell receptor α and β chains of CD4 + T-cells were analysed by flow cytometry, DNA-sequenced, and threedimensional molecular models of T-cell receptor-HLA-DRB1*03 complexes generated.Simultaneous expression of Vα2.3 with the Vβ22 chain was identified in the lungs of all HLA-DRB1*03 + patients. Accumulated Vα2.3/Vβ22-expressing T-cells were highly clonal, with identical or near-identical Vα2.3 chain sequences and inter-patient similarities in Vβ22 chain amino acid distribution. Molecular modelling revealed specific T-cell receptor-HLA-DRB1*03-peptide interactions, with a previously identified, sarcoidosis-associated vimentin peptide, (Vim)429-443 DSLPLVDTHSKRTLL, matching both the HLA peptide-binding cleft and distinct T-cell receptor features perfectly.We demonstrate, for the first time, the accumulation of large clonal populations of specific Vα2.3/Vβ22 T-cell receptor-expressing CD4 + T-cells in the lungs of HLA-DRB1*03 + sarcoidosis patients. Several distinct contact points between Vα2.3/Vβ22 receptors and HLA-DRB1*03 molecules suggest presentation of prototypic vimentin-derived peptides. @ERSpublications Clonal CD4 + lung T-cells associating with HLA-DRB1*03 molecules indicate specific antigens in pulmonary sarcoidosis

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Section: Vβ22supporting

confidence: 91%

T-cell receptor–HLA-DRB1 associations suggest specific antigens in pulmonary sarcoidosis

et al. 2015

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“…On the other hand, elevated CMV IgG titers were observed in sera of SLE patients. The data also supported the theory that EBV is associated with many autoimmune diseases and that CMV also appears to be associated with autoimmune diseases, although this theory requires further investigation [40][41][42]. Another report found that IgG and IgM isotypes of aCL were detected in CMV infections, with a high prevalence (56%) of aPL being reported in patients with CMV infection, although no association was found between these antibodies and the clinical expression of autoimmunity [36].…”

Section: Other Viral Infections and Antiphospholipid Antibodiessupporting

confidence: 69%

“…Another report found that IgG and IgM isotypes of aCL were detected in CMV infections, with a high prevalence (56%) of aPL being reported in patients with CMV infection, although no association was found between these antibodies and the clinical expression of autoimmunity [36]. Meyohas et al reported [43] that dual viral infection with CMV and HIV resulted in thrombotic manifestations of APS, including digital infarcts [41][42][43].…”

Section: Other Viral Infections and Antiphospholipid Antibodiesmentioning

confidence: 99%

Infections and the Antiphospholipid Syndrome

Garcı́a-Carrasco

Galarza-Maldonado

Mendoza‐Pinto³

et al. 2008

Clinic Rev Allerg Immunol

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Currently, the origin of autoimmune diseases is considered to be multifactorial. Genetic predisposition, immune system malfunction or even backfire, hormonal regulation, and environmental factors, i.e. infections, all play important roles in the pathogenesis of autoimmune diseases such as the antiphospholipid syndrome (APS). New drugs and strategies aimed at preventing infections could further improve the outcome of APS and other autoimmune diseases.

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“…While the association of aPL and smoking has been reported in studies of vascular events (as described above), the published reviews [8,9,86] describing the relationship of infections and aPL have not considered a possible association between aPL and smoking, possibly because of widespread support for the mimicry model.…”

Section: Periodontal Infections Smoking and Aplmentioning

confidence: 99%

“…These screening syphilis tests detect antibodies directed against cardiolipin, the same antigen used in the earliest screening tests for aPL [5,6]. The relationship between infections with aPL has been the subject of many studies and reviews [7][8][9]. The likelihood that an infectious disease can trigger catastrophic antiphospholipid syndrome has been frequently demonstrated [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Anti-phospholipid Antibodies and Smoking: An Overview

Binder

Litwin

2016

Clinic Rev Allerg Immunol

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Antiphospholipid syndrome is characterized by the presence of antiphospholipid antibodies, specifically lupus anticoagulant, anticardiolipin antibodies, and anti-β2 glycoprotein-I antibodies. Antiphospholipid syndrome can occur on its own or in association with other autoimmune diseases, most commonly systemic lupus erythematosus (SLE). A connection between cigarette smoking and anti-phospholipid antibodies (aPL) was first reported in the late1980s. Systemic lupus erythematosus patients with aPL are more likely to be smokers than those without aPL. These patients have a particularly high frequency of vascular events. Recently, a potential link between periodontitis, tobacco, and aPL has been proposed. Research has also suggested that periodontitis and Porphyromonas gingivalis infection are associated with citrullination through the action of peptidylarginine deiminase. A strong correlation between smoking and the presence of citrillunated autoantibodies, which are characteristic of rheumatoid arthritis, has also been observed. While many studies have investigated possible links between infection and aPL in patients with autoimmune diseases, the association of smoking with aPL has not been systematically examined. The fact that both aPL and tobacco are risk factors for thrombosis has complicated efforts to evaluate these factors separately. Also, there has been great variability in measurement techniques, and laboratories lack routine methods for differentiating transient and persistent aPL; both of these factors can make interpretation of autoantibody results quite challenging. This review summarizes the clinical evidence supporting a posited link between aPL and smoking, both in patients with a systemic autoimmune disease and in patients with other medical conditions.

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Antiphospholipid syndrome associated with infections: clinical and microbiological characteristics

Cited by 45 publications

References 57 publications

T-cell receptor–HLA-DRB1 associations suggest specific antigens in pulmonary sarcoidosis

T-cell receptor–HLA-DRB1 associations suggest specific antigens in pulmonary sarcoidosis

Infections and the Antiphospholipid Syndrome

Anti-phospholipid Antibodies and Smoking: An Overview

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