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short notes on new advances in the field

Activation of the Brain-Splenic Nerve Axis in Hypertension: The Cholinergic-Sympathetic-Immune System Connection

Activation of the Brain-Splenic Nerve Axis in Hypertension: The Cholinergic-Sympathetic-Immune System Connection

A recent Nature Communications study indicates that hypertension is linked to T cell activation and an egression of T-cells from the spleen, and that this process is dependent on a vagus-splenic nerve connection. Hypertension is a major risk factor for coronary heart diseases and stroke. Despite various therapeutic approaches 10-15% of the general hypertensive population […]

Sympathetic Nerves via β2-adrenoceptor Signaling Generate Circadian Rhythms and Govern Lymphocyte Recirculation in Lymph Nodes

Sympathetic Nerves via β2-adrenoceptor Signaling Generate Circadian Rhythms and Govern Lymphocyte Recirculation in Lymph Nodes

A new study, published in the Journal of Experimental Medicine (JEM), indicates that in mice, the sympathetic nervous system (SNS) innervation, through β2-adrenergic receptors activation controls the circadian dynamics and traffic of lymphocytes through the lymph nodes (LNs). Both primary and secondary lymphoid organs are heavily innervated, mostly by the peripheral sympathetic nerves. Thus, locally […]

New Function of Microglia: Promotion of Filopodia and Hence Synaptogenesis during Early Brain Development

New Function of Microglia: Promotion of Filopodia and Hence Synaptogenesis during Early Brain Development

A recent study published in Nature Communications reveals that the brain microglia influences the developing brain through induction of filopodia creation, thus, shaping neuronal connectivity and synapses formation. Microglia are important components of the neuro-immune interactions in the brain. As the resident macrophage cells, the microglial cells provide the main immune defense in the central […]

Adiponectin Enhances Th17 Actions and RANKL Expression Promoting Arthritis Inflammation and Bone Erosion

Adiponectin Enhances Th17 Actions and RANKL Expression Promoting Arthritis Inflammation and Bone Erosion

A study published in the online Scientific Reports journal reveals a new maladaptive and pro-inflammatory effect of adiponectin – its ability to increase T helper (Th)17 immune responses and the expression of receptor activator of nuclear factor-κB ligand (RANKL) in an animal model of arthritis. Adiponectin, a protein secreted mostly by adipocytes (fat cells),  is […]

Microglia and TREM2 Microglia-Specific Gene May Exert a Protective Role in Alzheimer´s Disease

Microglia and TREM2 Microglia-Specific Gene May Exert a Protective Role in Alzheimer´s Disease

A study published in the May issue of Neuron indicates that the brain microglia may exert a protective role in Alzheimer´s disease (AD) by tightly wrapping around the early amyloid fibrils and plaques endorsing their compaction and insulation. In Alzheimer´s disease two hallmark protein aggregates, amyloid-β (Aβ) plaques and neurofibrillary tangles are the major players […]

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 […]

The Th17–IL-17–IL-17R System Linked To Altered Brain Development and Autism-Like Symptoms in Mice

The Th17–IL-17–IL-17R System Linked To Altered Brain Development and Autism-Like Symptoms in Mice

A new report published in Science indicates that the key pro-inflammatory cytokine interleukin (IL)-17a may interfere with the normal brain development in a mouse model of autism, causing disorganized cortical cytoarchitecture and autism-like symptoms. IL-17 is a highly pathogenic pro-inflammatory cytokine, considered a major player in several autoimmune/inflammatory diseases, whereas altered cytokine profiles and increased […]

Sympathetic Nerves Keep Up an Anti-Inflammatory State by Inhibiting Macrophage TNF-α Expression in Fat Tissue

Sympathetic Nerves Keep Up an Anti-Inflammatory State by Inhibiting Macrophage TNF-α Expression in Fat Tissue

New report, published in Endocrinology, implicates the activity of the sympathetic nervous system (SNS) and its β2-adrenoceptor signaling pathway in sustaining at low levels the production of the pro-inflammatory cytokine tumor necrosis factor (TNF)-α in macrophages of lean mice. Pro-inflammatory macrophages play a key role in the pathogenesis of the systemic low-grade chronic inflammation, associated […]

First Evidence that IL-9 Contributes to Atherosclerosis Development

First Evidence that IL-9 Contributes to Atherosclerosis Development

Perhaps the first evidence for an involvement of IL-9 in atherosclerosis was recently reported in the online journal PLoS One by Ida Gregersen and colleagues from the Oslo University Hospital Rikshospitalet, Oslo, Norway. Interleukin (IL)-9 is a cytokine linked mostly to T helper (Th)2 cell responses and Th2-related conditions such as parasitic helminth infections and […]

Arthritis Protection By Estrogens: Driving Th17 Cells To Lymph Nodes But Restricting Their Migration to the Joints?

Arthritis Protection By Estrogens: Driving Th17 Cells To Lymph Nodes But Restricting Their Migration to the Joints?

Annica Andersson and colleagues from the Department of Rheumatology and Inflammation Research, University of Gothenburg, Gothenburg, Sweden published in Arthritis Research & Therapy a study indicating that the regulation exerted by estrogens, to the Th17 cell traffic and migration, may play an important role in the well established protective role of female hormones in rheumatoid […]

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