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Related Concept Videos

Autonomic Nervous System01:22

Autonomic Nervous System

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The autonomic nervous system (ANS) is a critical component of the peripheral nervous system, primarily responsible for regulating involuntary bodily functions and maintaining homeostasis. It functions in tandem with the central nervous system (CNS) to seamlessly coordinate various physiological processes without the need for conscious control.
The ANS comprises two main divisions: the sympathetic and parasympathetic divisions. These divisions function antagonistically to maintain a dynamic...
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Autonomic Nervous System: Overview01:26

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The human nervous system is divided into two main parts: the central nervous system (CNS) and the peripheral nervous system (PNS). The CNS is composed of the brain and spinal cord, while the PNS contains nerve cells, clusters of nerve cells, and the sensory receptors that are outside the CNS. The PNS has two types of nerve cells: sensory (afferent) and motor (efferent). Sensory cells send signals to the CNS from receptors, and motor cells carry signals from the CNS to organs, muscles, and...
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Disorders of the Autonomic Nervous System01:18

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The autonomic nervous system (ANS) is an intricate network of nerves that controls functions such as the regulation of heart rate, digestion, and blood pressure regulation. When this system malfunctions, it can lead to various disorders that affect multiple bodily functions. One common feature of many autonomic disorders is the involvement of smooth blood vessels, which play a crucial role in regulating blood flow throughout the body.
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Types of Hormones02:13

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Hormones can be classified into three main types based on their chemical structures: steroids, peptides, and amines. Their actions are mediated by the specific receptors they bind to on target cells.
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Drugs Acting on Autonomic Ganglia: Stimulants01:23

Drugs Acting on Autonomic Ganglia: Stimulants

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Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating...
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Drugs Acting on Autonomic Ganglia: Blockers01:28

Drugs Acting on Autonomic Ganglia: Blockers

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Ganglionic blockers inhibit autonomic activity by blocking nicotinic receptors in the autonomic ganglia, suppressing impulse transmission. These blockers lack selectivity between sympathetic and parasympathetic ganglia and are ineffective as neuromuscular junction antagonists. They can be categorized into two groups:
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Isolation, Transfection, and Culture of Primary Human Monocytes
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SAMHD1 deficient human monocytes autonomously trigger type I interferon.

Alicia Martinez-Lopez1, Marta Martin-Fernandez2, Sofija Buta2

  • 1Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, United States.

Molecular Immunology
|August 13, 2018
PubMed
Summary
This summary is machine-generated.

Germline mutations in the SAMHD1 gene cause Aicardi-Goutières Syndrome (AGS). SAMHD1 knockout cells show spontaneous type I interferon (IFN) production, driving disease pathogenesis.

Keywords:
AGSIFNISGsSAMHD1TBK1-IRF3

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Generation of Human Monocyte-derived Dendritic Cells from Whole Blood
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Area of Science:

  • Immunology
  • Genetics

Background:

  • Aicardi-Goutières Syndrome (AGS) is linked to germline mutations in the SAMHD1 gene.
  • A hallmark of AGS is elevated systemic type I interferon (IFN) production.

Purpose of the Study:

  • To investigate type I IFN induction and response in SAMHD1 knockout (KO) human monocytic cells.
  • To elucidate the molecular mechanisms underlying aberrant IFN production in SAMHD1 deficiency.

Main Methods:

  • Generated SAMHD1 knockout (KO) human monocytic cell lines.
  • Assessed IFN-β and interferon-stimulated gene (ISG) transcription and translation.
  • Utilized TBK1-IRF3 pathway inhibition and type I IFN blocking antibodies.

Main Results:

  • SAMHD1 KO cells exhibited spontaneous IFN-β and ISG production compared to wild-type cells.
  • Inhibition of the TBK1-IRF3 pathway abrogated IFN-β and ISG elevation in SAMHD1 KO cells.
  • SAMHD1 KO cells showed increased phosphorylated TBK1 and ISG levels were reversed by IFN-blocking antibodies.

Conclusions:

  • SAMHD1 deficiency leads to persistent auto-stimulation of the TBK1-IRF3 pathway.
  • This aberrant signaling results in enhanced type I IFN production and self-induction of ISGs.
  • Findings highlight the critical role of SAMHD1 in regulating innate immune responses and preventing autoinflammation.