June 29, 2022

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Immune cells can change behavior unexpectedly and cause psoriasis

Nature: Immune cells can change behavior unexpectedly and cause psoriasis

 

 

Nature: Immune cells can change behavior unexpectedly and cause psoriasis.   Studies have shown that when driven, certain types of immune cells change their behavior in unexpected ways, producing protein signals that cause damage.

  
Millions of people suffer from psoriasis, a chronic autoimmune disease that causes scaly patches on the skin. In order to improve treatment options, scientists need to better understand the immune system disorders that cause these diseases.

Researchers from the University of Chicago’s School of Molecular Engineering (PME) conducted advanced computational genomic analysis on immune cells in mouse models and found that when driven, certain immune cells change their behavior in unexpected ways, resulting in The protein signal of the disease.

This research, published in the journal Nature, completed by Dr. Samantha Riesenfeld and others, reveals a new way of immune response and may eventually lead to better disease treatments.

 

 


Understand the behavior of immune cells

This research was completed by researchers including Yale University, Massachusetts Institute of Technology, and Harvard University. They hope to better understand innate lymphoid cells (ILCs), which are found in barrier tissues such as the skin and intestinal lining. Of immune cells. Although this type of cell does not have as many studies as T cells (which play a central role in the body’s adaptive immune response), ILCs can quickly sense, integrate, respond and transmit signals, thereby regulating downstream immune responses.

Previous studies have observed a special type of ILCs in skin lesions and proposed their importance in driving psoriasis (psoriasis), but the origin of these ILCs and their role are still unclear. To find out their roles, the research team used a combination of experimental and computational methods.

In the experiment, the researchers used interleukin-23 (IL-23) to stimulate skin inflammation in a mouse model, a cytokine involved in causing psoriasis lesions. Even in mice lacking all T cells, ILCs can still cause psoriasis. In the process of disease induction, scientists isolated thousands of ILCs from mouse skin and analyzed the gene expression of these cells using single-cell RNA sequencing.

Then, Riesenfeld and others used machine learning technology to quantitatively model this high-dimensional gene expression data, and analyze the behavior of ILCs before and in response to IL-23 treatment.

Their model shows that ILCs in this range are plastic, allowing them to respond to IL-23 signals by changing programmed actions, and are generally considered to be a stable part of their identity, thereby producing pathogenic cytokines that induce skin damage. Scientists verified these predictions through experiments, using genetically modified mice that track the fate of ILC.

Riesenfeld said: “These findings provide us with new information about how psoriasis occurs and how inflammation changes the behavior of immune cells.” “We now think that the identity of ILCs cells is more flexible and less uncertain than we thought in the past. That is, cells that tend to play a role may do very different things under stress.”

 

 

A new way to understand the immune system

The method of combining experiments and calculations can be used not only to describe a gene or protein, but also to describe the entire transcription program of a single immune cell. Appropriate analysis can provide valuable insights for understanding the immune response pattern.

Riesenfeld said: “Understanding how heterogeneous cells are integrated and transformed by immune signals is critical to solving basic health-related problems, such as why one person responds to inflammation while another person can tolerate it.”

With an in-depth understanding of how these cells work, this study suggests that better psoriasis treatments may ultimately be necessary to prevent these early responders from becoming pathogenic cells.

 

 

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