Scientists from the La Jolla Institute for Immunology (LJI) in California analyzed more than 1.1 million immune cells from human lung tissue samples to better understand how pulmonary and autoimmune diseases develop and if there is overlap between the two. Their findings are detailed in the recent paper, “Tissue-Resident Immune Cells Drive Genetic Risk in Autoimmune and Lung Diseases,” published in Nature Immunology.
The specific immune cells in question reside in the lungs and are known as tissue-resident cells, which help protect the body from infection and disease. LJI researchers found that the cells can express genes that cause malfunction in the immune system and increase a person’s risk for developing lung and autoimmune conditions.
The large-scale dataset included lung tissue samples donated by 128 people who were newly diagnosed with lung cancer, undergoing surgery and enrolled in the Target Lung study, led by University of Liverpool Professor Christian H. Ottensmeier, MD, PhD.
Researchers used single-cell RNA sequencing to identify genes and analyze gene expression in the tissue-resistant immune cells of the provided samples. Multiple genes, including ZFP57, demonstrated colocalization between lung immune cells of several autoimmune diseases, the authors reported. This suggests “shared genetic mechanisms underlying the risk of disease,” they wrote.
In addition, the research team observed that tissue-resident immune cells in the lungs not only behave significantly different than those in blood, but the cells express genes differently in men versus women. Specifically, the researchers identified several inflammatory genes that are expressed more in females.
The study was included in the Database of Immune Cell Epigenomics (DICE) project, in which research links genetic variations to immune cell function and helps determine why some people are at greater risk of autoimmune, pulmonary and infectious diseases.
