. The lack of specific surface markers and the rarity of pathogenic astrocytes has made it difficult to study these cells and identify potential therapeutic targets for MS. In their publication, Clark and colleagues introduce a method called FIND-seq that allows for the in-depth transcriptomic analysis of single cells, including rare populations.){kind=link}
Iain C. Clark and colleagues recently published an article in Nature that describes a new method for studying astrocytes, a type of cell that plays a role in the development of multiple sclerosis (MS). The lack of specific surface markers and the rarity of pathogenic astrocytes has made it difficult to study these cells and identify potential therapeutic targets for MS. In their publication, Clark and colleagues introduce a method called FIND-seq that allows for the in-depth transcriptomic analysis of single cells, including rare populations. This method has been used to study the regulation of astrocytes in MS and has led to the identification of a potential therapeutic target. This publication is important because it presents a new tool for studying astrocytes and may provide insight into the development of treatments for MS.
Multiple sclerosis (MS) is a chronic autoimmune disorder that affects the central nervous system (CNS). Astrocytes, a type of glial cell found in the CNS, have been shown to play a role in the development of MS and a related condition called experimental autoimmune encephalomyelitis (EAE). However, it has been difficult to study astrocytes and identify potential therapeutic targets due to the lack of specific surface markers and the rarity of pathogenic astrocytes. To overcome these limitations, we developed FIND-seq, a microfluidic cytometry method that uses droplet encapsulation, PCR-based nucleic acid detection, and droplet sorting to enable single-cell transcriptomic analysis. Using FIND-seq in combination with various techniques including genetic perturbation and RNA sequencing, we studied the role of the transcription factor XBP1 in the regulation of astrocytes in MS and EAE. We found that the nuclear receptor NR3C2 and its corepressor NCOR2 play a role in limiting the harmful effects of XBP1 in astrocytes. Our findings demonstrate the utility of FIND-seq in studying rare cell populations and identifying potential therapeutic targets.