Publications by authors named "C Hoornaert"
Article Synopsis
- Multiple sclerosis (MS) is an autoimmune disease that damages myelin in the central nervous system, leading to injury of brain and spinal cord cells due to immune cell infiltration, particularly by pro-inflammatory Th17 cells.
- The study investigated how these Th17 cells interact with oligodendrocytes (the myelin-producing cells) through specific adhesion molecules, finding that the presence of certain molecules like ALCAM helps these cells adhere, which can lead to cell death.
- Results showed that in the presence of inflammatory cytokines or activated T cells, the expression of MCAM decreased, offering protective insights that targeting ALCAM could reduce harmful interactions between Th17 cells and oligodendrocytes, potentially leading to new therapeutic strategies for
Article Synopsis
- Multiple sclerosis (MS) is a complex disease involving immune cell infiltration into the central nervous system (CNS), but the exact mechanisms of this process are not well understood.
- This study used single-cell RNA sequencing and analyses of endothelial cells in an animal model of MS to uncover gene expression patterns related to neuroinflammation, particularly focusing on venous endothelial cells (ECs).
- Findings indicated that venous ECs play a significant role in neuroinflammation, with notable gene expression changes and molecular interactions identified, contributing to a better understanding of the processes that allow immune cells to enter the brain in MS.*
Oncostatin M (OSM) is an IL-6 family member which exerts neuroprotective and remyelination-promoting effects after damage to the central nervous system (CNS). However, the role of OSM in neuro-inflammation is poorly understood. Here, we investigated OSM's role in pathological events important for the neuro-inflammatory disorder multiple sclerosis (MS).
View Article and Find Full Text PDFObjective: To develop and validate a standardized Best Possible Medication History (BPMH) form that could be used by clinical pharmacists.
Methods: The draft version was presented to a focus group and was adapted following their comments. A three-rounds e-Delphi method was used to validate content, usability and face validity of the BPMH form.
The migration of circulating leukocytes into the central nervous system (CNS) is a key driver of multiple sclerosis (MS) pathogenesis. The monoclonal antibody natalizumab proved that pharmaceutically obstructing this process is an effective therapeutic approach for treating relapsing-remitting MS (RRMS). Unfortunately, the clinical efficacy of natalizumab is somewhat offset by its incapacity to control the progressive forms of MS (PMS) and by life-threatening side effects in RRMS rising from the expression of its molecular target, very late antigen 4 (VLA4), on most immune cells and consequent impairment of CNS immunosurveillance.
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