Publications by authors named "E Lindmark"

Background: The clinical-stage drug candidate EBL-1003 (apramycin) represents a distinct new subclass of aminoglycoside antibiotics for the treatment of drug-resistant infections. It has demonstrated best-in-class coverage of resistant isolates, and preclinical efficacy in lung infection models. However, preclinical evidence for its utility in other disease indications has yet to be provided.

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Autoimmune polyendocrine syndrome Type I (APS I) results in multiple endocrine organ destruction and is caused by mutations in the Autoimmune regulator gene (AIRE). In the thymic stroma, cells expressing the AIRE gene dictate T cell education and central tolerance. Although this function is the most studied, AIRE is also expressed in the periphery in DCs and stromal cells.

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Article Synopsis
  • Autoimmune polyendocrine syndrome type I (APS I) is caused by mutations in the AIRE gene, leading to destruction of multiple endocrine organs and increased levels of tissue-specific autoantibodies that predict organ damage.
  • In experiments with mice lacking AIRE (Aire(-/-)), there was an observed heightened B-cell response to T-cell-independent antigens, linked to higher levels of the B-cell-activating factor (BAFF), suggesting an immune dysfunction.
  • The research indicates that AIRE plays a critical role in regulating immune tolerance by affecting dendritic cell function and signaling, particularly through the response to IFN-gamma, which may help explain the mechanisms behind APS I.*
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Introduction: Mounting evidence implies beneficial properties of statins and angiotensin converting enzyme (ACE)-inhibitors beyond those of their original indications in the treatment of coronary artery disease (CAD). Less is known of the mechanisms by which low-molecular-weight (LMW) heparin, also used in unstable CAD, affects the cellular micro-environment. The effects of these drugs in monocyte-endothelial cell co-culture systems have so far been sparsely investigated.

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