Clues as to how inducible immune tissues arise in the lung are found in a report published online this week in Nature Immunology.
Patients with chronic obstructive pulmonary disease commonly exhibit clusters of immune cells that are collectively known as iBALT. Such clusters promote rapid immune responses to inhaled allergens or particles, such as soot or cigarette smoke, and can perpetuate chronic lung inflammation and lead to tissue damage.
Troy Randall and colleagues show that neonatal mice are exquisitely prone to development of iBALT structures upon exposure to inflammatory stimuli. They find that the signaling molecule IL-17 is essential to this process as it induces upregulation of specific chemoattractant molecules that leads to iBALT formation. These iBALT then persist for months via an IL-17-independent process involving another immune signaling molecule called lymphotoxin.
Strategies to block IL-17 and lymphotoxin might prove useful in therapeutics for chronic obstructive pulmonary disease or autoimmune diseases, such as Sjogren’s syndrome, that are associated aberrant formation of lymphoid tissues.