The mystery behind why inflammation still ravages lungs of some smokers who have kicked the habit years ago has been unraveled by scientists from Baylor College of Medicine.
They found that certain dendritic cells in the lung - the cells that "present" a foreign antigen or protein to the immune system - provoke production of destructive T-cells that attack a key protein called elastin, leading to death of lung tissue and emphysema.
Dr. Farrah Kheradmand, associate professor of medicine - pulmonary and immunology at BCM, has already shown that T-helper cells and some enzymes in the lung destroyed tissue in the lungs of emphysema patients.
She found that a subset of antigen-presenting cells in the lung are programmed to turn peripheral blood cells into the cells that are activated and are associated with autoimmune inflammation.
They also found that elastin peptides can activate T cells -a sign that elastin is acting as an auto-antigen.
"This has implications for something that is important and biologically relevant," said Kheradmand.
"Smokers are also at risk for diseases of the blood vessels such as the carotid artery and aorta. These blood vessels are also enriched in elastin. We believe that particular cells circulating in the body could react to elastin molecule at these remote sites," she added.
This may help explain some of the cardiovascular and other complications associated with smoking tobacco. For example, skin is rich in elastin. The skin of smokers loses elasticity.
"The Holy Grail is to find smokers who are destined to develop auto-reactive cells before the disease is fully manifested," she said.
She said they hope to come with a test for T-cells that attack elastin that could be used in the doctor's office. However, she said, such a test would only identify patients at higher risk for emphysema and other elastin-associated diseases. It would not identify people at higher risk of lung cancer, for example.
The work appears in the current issue of Science Transformational Medicine.