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A highlight from the LUPUS 2014 meeting: eight great ideas.

Buyon JP, Cohen P, Merrill JT, Gilkeson G, Kaplan M, James J, McCune WJ, Bernatsky S, Elkon K - Lupus Sci Med (2015)

Bottom Line: This review describes eight 'great ideas' regarding bench-to-bedside considerations in systemic lupus erythematosus (SLE) presented at the second international LUPUS meeting in Quebec, September 2014.The topics included: correcting the impaired clearance of apoptotic fragments; optimisation of clinical trial design: the PERFECT (Pre Evaluation Reducing Frighteningly Elevated Coverable Targets) study; lipidomics and metabolomics in SLE; importance of the inflammasome; identification and treatment of asymptomatic autoimmunity: prevention of SLE; combining low doses of hydroxychloroquine and quinacrine for long-term maintenance therapy of SLE; reducing emergency room visits and the critical relevance of the autoantigen.

View Article: PubMed Central - PubMed

Affiliation: Division of Rheumatology, Department of Medicine , NYU School of Medicine , New York, New York , USA.

ABSTRACT
This review describes eight 'great ideas' regarding bench-to-bedside considerations in systemic lupus erythematosus (SLE) presented at the second international LUPUS meeting in Quebec, September 2014. The topics included: correcting the impaired clearance of apoptotic fragments; optimisation of clinical trial design: the PERFECT (Pre Evaluation Reducing Frighteningly Elevated Coverable Targets) study; lipidomics and metabolomics in SLE; importance of the inflammasome; identification and treatment of asymptomatic autoimmunity: prevention of SLE; combining low doses of hydroxychloroquine and quinacrine for long-term maintenance therapy of SLE; reducing emergency room visits and the critical relevance of the autoantigen.

No MeSH data available.


Related in: MedlinePlus

Celiac disease as a model for SLE. In celiac disease, both the trigger (gluten) and drivers (activated T and B memory cells) lead to production of autoantibodies (in this case targeted to transglutaminase 2) (left panel). If the offending external antigen is removed, the disease goes into remission but persistence of memory T and B cells renders patients exquisitely sensitive to exacerbations of disease upon re-exposure to antigen. In SLE (right panel) the dominant site of antigenic stimulation is proposed to be skin rather than gut. Here, UV light acts as the trigger. In contrast to cytotoxic CD8 T cells in celiac, the key driver in SLE is memory B cells but T cells may also play a role. (Figure modified from Ludvig et al. Nat Rev Immunol 2013;13:294–303)
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LUPUS2015000087F4: Celiac disease as a model for SLE. In celiac disease, both the trigger (gluten) and drivers (activated T and B memory cells) lead to production of autoantibodies (in this case targeted to transglutaminase 2) (left panel). If the offending external antigen is removed, the disease goes into remission but persistence of memory T and B cells renders patients exquisitely sensitive to exacerbations of disease upon re-exposure to antigen. In SLE (right panel) the dominant site of antigenic stimulation is proposed to be skin rather than gut. Here, UV light acts as the trigger. In contrast to cytotoxic CD8 T cells in celiac, the key driver in SLE is memory B cells but T cells may also play a role. (Figure modified from Ludvig et al. Nat Rev Immunol 2013;13:294–303)

Mentions: KE reasoned using coeliac disease as a model where both the trigger (gluten) and drivers (activated T and B memory cells) lead to production of autoantibodies (in this case targeted to transglutaminase 2) (figure 4, left panel). The remarkable observation is if the trigger—the offending external antigen—is removed, the disease goes into remission. Note that survival of memory T and B cells renders patients exquisitely sensitive to exacerbations of disease upon re-exposure to antigen.


A highlight from the LUPUS 2014 meeting: eight great ideas.

Buyon JP, Cohen P, Merrill JT, Gilkeson G, Kaplan M, James J, McCune WJ, Bernatsky S, Elkon K - Lupus Sci Med (2015)

Celiac disease as a model for SLE. In celiac disease, both the trigger (gluten) and drivers (activated T and B memory cells) lead to production of autoantibodies (in this case targeted to transglutaminase 2) (left panel). If the offending external antigen is removed, the disease goes into remission but persistence of memory T and B cells renders patients exquisitely sensitive to exacerbations of disease upon re-exposure to antigen. In SLE (right panel) the dominant site of antigenic stimulation is proposed to be skin rather than gut. Here, UV light acts as the trigger. In contrast to cytotoxic CD8 T cells in celiac, the key driver in SLE is memory B cells but T cells may also play a role. (Figure modified from Ludvig et al. Nat Rev Immunol 2013;13:294–303)
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4493165&req=5

LUPUS2015000087F4: Celiac disease as a model for SLE. In celiac disease, both the trigger (gluten) and drivers (activated T and B memory cells) lead to production of autoantibodies (in this case targeted to transglutaminase 2) (left panel). If the offending external antigen is removed, the disease goes into remission but persistence of memory T and B cells renders patients exquisitely sensitive to exacerbations of disease upon re-exposure to antigen. In SLE (right panel) the dominant site of antigenic stimulation is proposed to be skin rather than gut. Here, UV light acts as the trigger. In contrast to cytotoxic CD8 T cells in celiac, the key driver in SLE is memory B cells but T cells may also play a role. (Figure modified from Ludvig et al. Nat Rev Immunol 2013;13:294–303)
Mentions: KE reasoned using coeliac disease as a model where both the trigger (gluten) and drivers (activated T and B memory cells) lead to production of autoantibodies (in this case targeted to transglutaminase 2) (figure 4, left panel). The remarkable observation is if the trigger—the offending external antigen—is removed, the disease goes into remission. Note that survival of memory T and B cells renders patients exquisitely sensitive to exacerbations of disease upon re-exposure to antigen.

Bottom Line: This review describes eight 'great ideas' regarding bench-to-bedside considerations in systemic lupus erythematosus (SLE) presented at the second international LUPUS meeting in Quebec, September 2014.The topics included: correcting the impaired clearance of apoptotic fragments; optimisation of clinical trial design: the PERFECT (Pre Evaluation Reducing Frighteningly Elevated Coverable Targets) study; lipidomics and metabolomics in SLE; importance of the inflammasome; identification and treatment of asymptomatic autoimmunity: prevention of SLE; combining low doses of hydroxychloroquine and quinacrine for long-term maintenance therapy of SLE; reducing emergency room visits and the critical relevance of the autoantigen.

View Article: PubMed Central - PubMed

Affiliation: Division of Rheumatology, Department of Medicine , NYU School of Medicine , New York, New York , USA.

ABSTRACT
This review describes eight 'great ideas' regarding bench-to-bedside considerations in systemic lupus erythematosus (SLE) presented at the second international LUPUS meeting in Quebec, September 2014. The topics included: correcting the impaired clearance of apoptotic fragments; optimisation of clinical trial design: the PERFECT (Pre Evaluation Reducing Frighteningly Elevated Coverable Targets) study; lipidomics and metabolomics in SLE; importance of the inflammasome; identification and treatment of asymptomatic autoimmunity: prevention of SLE; combining low doses of hydroxychloroquine and quinacrine for long-term maintenance therapy of SLE; reducing emergency room visits and the critical relevance of the autoantigen.

No MeSH data available.


Related in: MedlinePlus