Researchers have shown that some immune diseases like asthma, multiple sclerosis, and arthritis are linked with the activation of certain types of cells called the memory T cells -- an advance that may lead to new drug targets for the treatment of these disorders.
The study, published in the journal Nature Genetics, could help narrow down the search for the chemical pathways behind immune diseases.
In some cases, the immune system that wards off infections and keeps us healthy can wrongly cause inflammation, leading to diseases such as asthma, multiple sclerosis, and inflammatory bowel disease (IBD), the study noted.
However, the researchers including those from the Sanger Institute in the US said that neither the triggers that cause the immune system to respond in this way, nor the exact cell types involved in the process are known.
Previous research, according to the study, found that there are thousands of genetic changes (known as genetic variants) that are more common among patients with immune diseases than in healthy people.
The study noted that understanding these genetic changes could provide clues to the causes and biological pathways involved in immune disease, and lead to identifying new drug targets.
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According to the researchers, many of these genetic variants are in poorly understood areas of the human genome, and are thought to be involved in regulating functions of immune cells.
They added that the involvement of small signalling proteins -- cytokines -- that allow communication between the immune cells during inflammation makes the process even more complex.
The researchers tried to understand the activity of the immune cells that are the most important for such diseases.
They cross-checked parts of the genome that was active in three types of immune cells between healthy volunteers and all the genetic variants implicated in the immune diseases.
The study revealed that one particular cell type and state -- early activation of memory T cells -- had the most active role in the genetic variants implicated in immune diseases.
According to the researchers, the initial activation of these cells is important in disease development.
The research also showed that cytokines generally only had weak effects on the activity of the DNA, and played a lesser role in most of the immune diseases studied.
"Our study is the first in depth analysis of immune cells and cytokine signals in the context of genetic differences linked to immune diseases," said Blagoje Soskic, a lead author on the paper from the Wellcome Sanger Institute.
According to Soskic, the links found between the disease variants and early activation of memory T cells suggested that the problems with regulating this process could lead to immune diseases.
The researchers mentioned that with thousands of different cell types and states in the body, finding the cause of autoimmune diseases was like finding a needle in a haystack.
"We have identified early activation of memory T cells as being particularly relevant to immune diseases, and will now be able to dive deeper into studying how this is regulated, to discover genes and pathways that could be used as drug targets," said Gosia Trynka, the senior author of the study from the Wellcome Sanger Institute.