Joyce Rauch

The antiphospholipid syndrome.

Phagocytosis of apoptotic cells by macrophages induces novel signaling events leading to cytokine-independent survival and inhibition of proliferation: activation of Akt and inhibition of extracellular signal-regulated kinases 1 and 2.

Factor V Leiden, prothrombin gene mutation, and thrombosis risk in patients with antiphospholipid antibodies.

Association of autoantibodies to nuclear lamin B1 with thromboprotection in systemic lupus erythematosus: lack of evidence for a direct role of lamin B1 in apoptotic blebs.

Prothrombin binds to the surface of apoptotic, but not viable, cells and serves as a target of lupus anticoagulant autoantibodies.

Thromboembolic risk in patients with high titre anticardiolipin and multiple antiphospholipid antibodies.

Structural features of the acyl chain determine self-phospholipid antigen recognition by a CD1d-restricted invariant NKT (iNKT) cell.

The presence of multiple prothrombotic risk factors is associated with a higher risk of thrombosis in individuals with anticardiolipin antibodies.

Induction of autoantibodies during prolonged treatment with infliximab.

Anti-phospholipid antibodies (aPL) and apoptosis: prothrombin-dependent aPL as a paradigm for phospholipid-dependent interactions with apoptotic cells.

Antiphospholipid antibodies and thrombosis: association with acquired activated protein C resistance in venous thrombosis and with hyperhomocysteinemia in arterial thrombosis.

Apoptotic cells, at all stages of the death process, trigger characteristic signaling events that are divergent from and dominant over those triggered by necrotic cells: Implications for the delayed clearance model of autoimmunity.

Immunization with an apoptotic cell-binding protein recapitulates the nephritis and sequential autoantibody emergence of systemic lupus erythematosus.

The antiphospholipid syndrome.

The affirmative response of the innate immune system to apoptotic cells.

Antiphospholipid antibodies predict imminent vascular events independently from other risk factors in a prospective cohort.

Altered cell-cell and cell-matrix interactions in the development of systemic autoimmunity.

T cells demonstrate a Th1-biased response to native beta2-glycoprotein I in a murine model of anti-phospholipid antibody induction.

Apoptotic and necrotic cells as sentinels of local tissue stress and inflammation: response pathways initiated in nearby viable cells.

Recognition of apoptotic cells by epithelial cells: conserved versus tissue-specific signaling responses.

Macrophages from lupus-prone MRL mice have a conditional signaling abnormality that leads to dysregulated expression of numerous genes.

Cardiolipin binds to CD1d and stimulates CD1d-restricted γδ T cells in the normal murine repertoire.

Association of autoantibodies to heat-shock protein 60 with arterial vascular events in patients with antiphospholipid antibodies.

Interaction of β2-glycoprotein I with lipopolysaccharide leads to Toll-like receptor 4 (TLR4)-dependent activation of macrophages.

Recognition-dependent signaling events in response to apoptotic targets inhibit epithelial cell viability by multiple mechanisms: implications for non-immune tissue homeostasis.

A polymorphism in TLR2 is associated with arterial thrombosis in a multi-ethnic SLE population.

β2-Glycoprotein I-specific T cells are associated with epitope spread to lupus-related autoantibodies.

Autoimmunity and antibody affinity maturation are modulated by genetic variants on mouse chromosome 12.

Apoptotic cells activate AMP-activated protein kinase (AMPK) and inhibit epithelial cell growth without change in intracellular energy stores.