Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Complement System

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...

Detergent Purification of Membrane Proteins

Detergent Purification of Membrane Proteins

Detergents are used to purify the integral proteins of the membrane. The hydrophobic portion of the detergent can replace membrane phospholipids while solubilizing the membrane proteins. When detergent monomers reach a specific concentration in a solution called critical micelle concentration (CMC), they form micelles. Above CMC, the concentration of the detergent monomers remains in equilibrium with the micelle. The number of detergent monomers present in the CMC varies for each detergent, and...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Author Correction: Fc-engineered large molecules targeting blood-brain barrier transferrin receptor and CD98hc have distinct central nervous system and peripheral biodistribution.

Nature communications·2026

Same author

Therapeutic targeting of neuroimmune mechanisms in neurodegeneration.

Nature reviews. Drug discovery·2026

Same author

TREM2 expression level is critical for microglial state, metabolic capacity and efficacy of TREM2 agonism.

Nature communications·2026

Same author

Loss of PILRA promotes microglial immunometabolism to reduce amyloid pathology in cell and mouse models of Alzheimer's disease.

Science translational medicine·2025

Same author

Early intervention anti-Aβ immunotherapy attenuates microglial activation without inducing exhaustion at residual plaques.

Molecular neurodegeneration·2025

Same author

Investigational eIF2B activator DNL343 modulates the integrated stress response in preclinical models of TDP-43 pathology and individuals with ALS in a randomized clinical trial.

Nature communications·2025

Same journal

Targeting cholesterol esterification sensitizes liver cancer to CD8<sup>+</sup> T cell attack by impairing metabolic and redox resilience.

Immunity·2026

Same journal

Brain endothelial cells orchestrate a neuroprotective antiviral state in the CNS in response to peripheral viral pattern sensing.

Immunity·2026

Same journal

Extracellular ATP-P2RY2 signaling drives intratumoral prostaglandin E2 accumulation and adaptive resistance to immunotherapy in solid tumors.

Immunity·2026

Same journal

B cell-derived type I interferon sustains T cell functionality upon strong TCR stimulation during chronic infection.

Immunity·2026

Same journal

Lactate binds and inhibits the innate immune sensor STING to promote tumor immune evasion.

Immunity·2026

Same journal

Antibody binding geometry and affinity control inhibitory hFcγRIIB receptor signaling.

Immunity·2026

See all related articles

Search research articles

Related Experiment Video

Updated: Jul 19, 2025

Efficient Mammalian Cell Expression and Single-step Purification of Extracellular Glycoproteins for Crystallization

Efficient Mammalian Cell Expression and Single-step Purification of Extracellular Glycoproteins for Crystallization

Published on: December 23, 2015

Cleaning crew: Soluble TREM2 mops up complement.

Kathryn M Monroe¹, Joseph W Lewcock¹

¹Denali Therapeutics Inc., South San Francisco, CA 94080, USA.

|August 9, 2023

Summary

This summary is machine-generated.

Soluble TREM2 (triggering receptor expressed on myeloid cells 2) plays a key role in the brain. This study shows it prevents harmful synaptic pruning by binding to complement factor C1q, thus protecting neurons and reducing neurodegeneration.

More Related Videos

A Microplate Assay to Assess Chemical Effects on RBL-2H3 Mast Cell Degranulation: Effects of Triclosan without Use of an Organic Solvent

A Microplate Assay to Assess Chemical Effects on RBL-2H3 Mast Cell Degranulation: Effects of Triclosan without Use of an Organic Solvent

Published on: November 1, 2013

Measuring the 50% Haemolytic Complement CH50 Activity of Serum

Measuring the 50% Haemolytic Complement CH50 Activity of Serum

Published on: March 29, 2010

Related Experiment Videos

Last Updated: Jul 19, 2025

Efficient Mammalian Cell Expression and Single-step Purification of Extracellular Glycoproteins for Crystallization

Efficient Mammalian Cell Expression and Single-step Purification of Extracellular Glycoproteins for Crystallization

Published on: December 23, 2015

A Microplate Assay to Assess Chemical Effects on RBL-2H3 Mast Cell Degranulation: Effects of Triclosan without Use of an Organic Solvent

A Microplate Assay to Assess Chemical Effects on RBL-2H3 Mast Cell Degranulation: Effects of Triclosan without Use of an Organic Solvent

Published on: November 1, 2013

Measuring the 50% Haemolytic Complement CH50 Activity of Serum

Measuring the 50% Haemolytic Complement CH50 Activity of Serum

Published on: March 29, 2010

Area of Science:

Neuroscience
Immunology
Molecular Biology

Background:

The function of soluble TREM2 (triggering receptor expressed on myeloid cells 2) in the central nervous system remains largely unknown.
Synaptic pruning is a critical process in neural development and plasticity, but aberrant pruning can contribute to neurodegenerative diseases.

Purpose of the Study:

To investigate the functional role of soluble TREM2 in the central nervous system.
To determine the mechanism by which soluble TREM2 influences synaptic pruning and neuroprotection.

Main Methods:

The study utilized in vitro assays and in vivo models to examine the interaction between soluble TREM2 and complement factor C1q.
Researchers assessed the impact of soluble TREM2 on synaptic pruning and neuronal survival in the context of neurodegeneration.

Main Results:

Soluble TREM2 was found to bind to complement factor C1q, a key initiator of the classical complement pathway.
This binding effectively inhibited aberrant synaptic pruning mediated by C1q.
The inhibition of aberrant synaptic pruning by soluble TREM2 led to enhanced neuronal protection and mitigation of neurodegeneration.

Conclusions:

Soluble TREM2 has a critical neuroprotective function in the central nervous system.
By sequestering C1q, soluble TREM2 prevents excessive synaptic elimination, thereby safeguarding neuronal integrity.
These findings highlight soluble TREM2 as a potential therapeutic target for neurodegenerative disorders.