multiple sclerosis

Glucocorticoid-Resistant IL-17- and IL-22-secreting CD4+ T Cells May Contribute to Increased Disease Activity in Multiple Sclerosis

Glucocorticoid-Resistant IL-17- and IL-22-secreting CD4+ T Cells May Contribute to Increased Disease Activity in Multiple Sclerosis

A recent study published in Immunology is perhaps the first to demonstrate a correlation between the production of interleukin (IL)-17 and IL-22, and its glucocorticoid resistance, and the number of active brain lesions in multiple sclerosis (MS). Increased active brain lesions were found in patients whose IL-17- and IL-22-producing T cells were more resistant to […]

Th17 Cells and Lymphotoxin: Conductors for the Tertiary Lymphoid Tissues and Inflammation Orchestra

Th17 Cells and Lymphotoxin: Conductors for the Tertiary Lymphoid Tissues and Inflammation Orchestra

Commentary on the study by Natalia Pikor et al., Immunity, 2015, 43:1160-73. doi: 10.1016/j.immuni.2015.11.010 Integration of Th17- and Lymphotoxin-Derived Signals Initiates Meningeal-Resident Stromal Cell Remodeling to Propagate Neuroinflammation Tertiary lymphoid organs, or more properly, tertiary lymphoid tissues (TLTs), are accumulations of lymphoid tissues that arise in situations of chronic inflammation. TLTs have been shown to […]

TLRs-Activated Microglia Polarizes γδ T Cells towards a Neurotoxic IL-17+ γδ T Cell Phenotype: Implications for Multiple Sclerosis, Stroke and Alzheimer´s Disease

TLRs-Activated Microglia Polarizes γδ T Cells towards a Neurotoxic IL-17+ γδ T Cell Phenotype: Implications for Multiple Sclerosis, Stroke and Alzheimer´s Disease

A recent PLoS One study indicates that the cross-talk between the brain microglia and T cells that follows a microglia’s activation via Toll-like receptors (TLRs) stimulation, results in a shift of the T cells’ profile towards a neurotoxic IL-17+ γδ T cells phenotype. After the discovery of T helper (Th)17 cells in 2005, their main […]

Th17 Cells and Lymphotoxin Promote Tertiary Lymphoid Tissues Formation and Neuroinflammation

Th17 Cells and Lymphotoxin Promote Tertiary Lymphoid Tissues Formation and Neuroinflammation

According to a recent study published in Immunity, T helper (Th)17 cells initiate tertiary lymphoid tissues (TLTs) development in the meninges and propagate brain neuroinflammation. Tertiary lymphoid tissues or tertiary lymphoid organs (TLOs) represent accumulations of lymphoid cells at ectopic sites (in contrast to most lymphoid tissues developing before birth) usually triggered by chronic inflammation. […]

Melatonin May Control the Balance between Pathogenic Th17 and Regulatory T Cells

Melatonin May Control the Balance between Pathogenic Th17 and Regulatory T Cells

Commentary on the study by Mauricio Farez et al., 2015, Cell, 162, 1338–1352 Melatonin Contributes to the Seasonality of Multiple Sclerosis Relapses‘ The central master circadian clock is located in the suprachiasmatic nucleus (SCN). The output of this system is synchronized to 24 hours by the light-dark cycle. The SCN regulates rhythms in peripheral cells via […]

Further Evidence That the Cytokine GM-CSF is an Essential Factor in the Pathogenesis of Multiple Sclerosis

Further Evidence That the Cytokine GM-CSF is an Essential Factor in the Pathogenesis of Multiple Sclerosis

Rasouli et al., published in the June 1st issue of the Journal of Immunology reports that treatment-naive MS patients had greater numbers of GM-CSF+ T cells in the peripheral blood, whereas CD4+ and CD8+ T cells in MS brain lesions expressed GM-CSF. In addition, interferon (INF)-β suppressed GM-CSF production by T cells, in vitro conditions. […]

New Subset of T Helper Cells May Play a Critical Role in Multiple Sclerosis

New Subset of T Helper Cells May Play a Critical Role in Multiple Sclerosis

A study by Wanqiang Sheng and colleagues from the National University of Singapore, published in Cell Research identifies a new subset of T helper (Th) cells that may play a key role in autoimmune neuroinflammatory conditions such as multiple sclerosis. Recent evidence indicates that granulocyte-macrophage colony-stimulating factor (GM-CSF) is a major encephalitogenic factor contributing to […]