Findings by Swedish team of investigators could help identify biomarkers that would predict the response to treatments.
Inflammatory bowel disease (IBD) including ulcerative colitis, can affect children as well as adults. In fact, up to 25% of people living with IBD are diagnosed as children or adolescents, and this number is increasing. Childhood-onset IBD generally manifests with more severe symptoms and more extensive disease compared with adult-onset disease.
Little is known about the differences in the immune response of children with IBD versus that of adults with the same condition. It is known, however, that close to 40% of children and adults with IBD do not respond to currently available treatments. Identifying new biomarkers to help predict response to treatment is essential in the development of new therapies.
In a study published last month in the journal Cell Reports Medicine, researchers from Karolinska Institutet and Sachs’ Children and Youth Hospital in Stockholm, Sweden, mapped the immune system of the gut in children with IBD in an effort to better understand the inflammatory process of pediatric IBD.
Senior author Jenny Mjösberg, professor of tissue immunology at the Department of Medicine at Karolinska Institutet, and colleagues used flow cytometry and single-cell RNA sequencing to analyze immune cells from the gut of 25 children and eight adults with IBD and 10 children and eight adults without the disease.
Mjösberg and her colleagues found that children with IBD had more pro-inflammatory cells, such as innate lymphoid cells type 1 (ILC1), T cells, and natural killer (NK) cells, than adults. In addition, protective cells, such as type 3 innate lymphoid cells (ILC3) and tissue-resident T cells, were less prominent in the gut of children with IBD compared with adults.
The researchers hope that their results catalyze further research that will aid in the development of more targeted therapies for people with IBD, including children.
“Further mechanistic studies are necessary to understand whether and how these findings contribute to pathogenesis and how they could facilitate the design of immunotherapeutic targets,” they concluded.