The Role of the Gut Microbiota in the Pathogenesis of Antiphospholipid Syndrome

Ruff, William; Vieira, Sílvio M.; Kriegel, Martin

doi:10.1007/s11926-014-0472-1

Cited by 35 publications

(35 citation statements)

References 108 publications

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“…Gut microbiota is indeed increasingly recognized as a major player in the development of autoimmunity; commensal bacteria might contribute to APS pathogenesis inducing autoreactive CD4 þ T cells and antib2GPI antibody production, via molecular mimicry mechanisms or favouring conformational changes in b2GPI, ultimately inducing autoantibody production. Consistent evidence comes from in-vivo models: depletion of gut microbiome with broadspectrum antibiotics in APS-prone animals markedly prevented thrombotic events, increased survival and reduced anti-b2GPI IgG titres [15].…”

Section: Key Pointsmentioning

confidence: 80%

Update on the pathogenesis and treatment of the antiphospholipid syndrome

Chighizola

Raschi

Borghi

et al. 2015

Current Opinion in Rheumatology

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Section: Key Pointsmentioning

confidence: 80%

Update on the pathogenesis and treatment of the antiphospholipid syndrome

Chighizola

Raschi

Borghi

et al. 2015

Current Opinion in Rheumatology

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“…Furthermore, T cell receptors exhibit a high degree of cross-reactivity, 38 and several autoantigen-specific Abs and T cell receptors are crossreactive towards commensal antigens. 39,40 Systemic tolerance to microbiota-derived antigens may prevent autoimmunity to crossreactive autoantigens.…”

Section: Discussionmentioning

confidence: 99%

Subcellular antigen localization in commensal E. coli is critical for T cell activation and induction of specific tolerance

et al. 2019

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Oral tolerance to soluble antigens is critically important for the maintenance of immunological homeostasis in the gut. The mechanisms of tolerance induction to antigens of the gut microbiota are still less well understood. Here, we investigate whether the subcellular localization of antigens within non-pathogenic E. coli has a role for its ability to induce antigen-specific tolerance. E. coli that express an ovalbumin (OVA) peptide in the cytoplasm, at the outer membrane or as secreted protein were generated. Intestinal colonization of mice with non-pathogenic E. coli expressing OVA at the membrane induced the expansion of antigenspecific Foxp3 + T regs and mediated systemic immune tolerance. In contrast, cytoplasmic OVA was ignored by antigen-specific CD4 + T cells and failed to induce tolerance. In vitro experiments revealed that surface-displayed OVA of viable E. coli was about two times of magnitude more efficient to activate antigen-specific CD4 + T cells than soluble antigens, surface-displayed antigens of heat-killed E. coli or cytoplasmic antigen of viable or heat-killed E. coli. This effect was independent of the antigen uptake efficiency in dendritic cells. In summary, our results show that subcellular antigen localization in viable E. coli strongly influences antigenspecific CD4 + cell expansion and tolerance induction upon intestinal colonization.

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“…Several studies have proposed an infectious etiology of APS based upon molecular mimicry [81][82][83]. A role for vaccines in the generation of APS has been proposed [84], and recently, a microbiotic model for the genesis of APS has been presented [85].…”

Section: Periodontal Infections Smoking and Aplmentioning

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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The Role of the Gut Microbiota in the Pathogenesis of Antiphospholipid Syndrome

Cited by 35 publications

References 108 publications

Update on the pathogenesis and treatment of the antiphospholipid syndrome

Update on the pathogenesis and treatment of the antiphospholipid syndrome

Subcellular antigen localization in commensal E. coli is critical for T cell activation and induction of specific tolerance

Anti-phospholipid Antibodies and Smoking: An Overview

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