Smoking can kill off the immune cells that commonly protect people from multiple sclerosis (MS) and other autoimmune diseases, say researchers at the University of Copenhagen — a finding that may lead to new ways of treating such illnesses.
“It is clear that smoking is detrimental to overall health and can predispose to many diseases,” the journal’s deputy editor, John Wherry, said in a press release. “These new studies shed light on how smoking can also influence the immune system, an effect that may have implications in autoimmunity and also in other settings such as cancer and chronic inflammatory diseases.”
Researchers measured the levels of several immune cell populations in 16 healthy, non-smoking individuals and compared them with those of 16 smokers. They found that smokers had higher blood cell counts of granulocytes, monocytes and lymphocytes, though none of these immune cell subsets were associated with increased inflammatory or autoreactive response.
Authors also found that smokers had lower blood levels of mucosal-associated invariant T (MAIT) cells compared with nonsmokers.
To evaluate if smoke exposure could modulate immune cell populations in MS patients as it did in the healthy cohort, authors analyzed data from 76 MS patients (including 20 with relapsing-remitting MS, 28 with secondary progressive MS, and 28 with primary progressive MS).
The team confirmed that smoke exposure did indeed reduce levels of MAIT cells in MS patients, while non-smoking participants with MS had MAIT levels similar to those observed in healthy non-smoking individuals.
“We believe that our study represents an important contribution to the understanding of systemic immune cell alterations in smokers,” said Cecilie Ammitzbøll, the study’s lead author. She and other researchers couldn’t find any link between the immune cell subsets modulation caused by smoke and MS-associated risk factors such as HLA-DRB1, HLA-A2 and NAT1 gene mutations.
Ammitzbøll added: “We hope that focused research in specific cell populations might reveal pathogenic mechanisms contributing to the understanding of diseases associated with smoking.”