The condition, often known as atherosclerosis, is caused by the gradual hardening and narrowing of blood vessels due to the build-up of “bad” cholesterol deposits inside the vessel walls.
This build-up provokes an immune response but the white blood cells sent to fight the cholesterol combine with the invaders to inflame the vessel walls and form a plaque, narrowing the artery.
The condition can go unnoticed and be trouble-free for years, until the narrowing becomes too great and damages organs or a piece of the plaque.
When it is degraded by immune cells, it breaks off and is carried in the blood stream where it blocks smaller vessels, resulting in ischaemic stroke or heart attack, experts have said.
While the reasons for the build-up of plaques in vessel walls are not fully understood, the process begins from an early age and is thought to be a natural part of ageing.
Poor diet, smoking, hypertension, diabetes and obesity can accelerate atherosclerosis but increasingly researchers have been scrutinising the role the systemic immune response plays in exacerbating the condition.
The latest study, published in the journal Immunity and led by Ludwig-Maximilians-University of Munich academics in collaboration with Glasgow University, found that during ageing, immune cells infiltrate the blood vessel walls and form tertiary lymphoid organs (TLOs) next to plaque sites that appear to protect against atherosclerosis.
TLOs are similar to other lymph organs such as the tonsils, spleen and lymph nodes – key elements in the immune system.
But unlike these organs, which develop at specific locations in the embryo during gestation in the womb, TLOs develop during adult life in response to chronic inflammation.
Professor Andreas Habenicht, of Ludwig-Maximilians-University, said: “The impact of TLOs in any disease setting has been an important yet unanswered question in the immunology of unresolving inflammation.
“Our study suggests that the TLOs seem to provide protection from advanced athero- sclerosis.
“The ageing immune system assembles and selectively employs a TLO within diseased peripheral tissue to control immune responses, while bypassing the lymphoid organs including the spleen and lymph nodes.
“Thus, artery TLOs are instrumental to understanding adaptive immunity in advanced atherosclerosis and possibly other chronic inflammatory diseases, and key to identifying new targets for therapeutic intervention.”
Doctor Pasquale Maffia, of the Institute of Infection, Immunity and Inflammation at Glasgow University, said: “If we can translate our findings to humans, it would change the way we treat this condition in the advanced stages.”
The work was supported by the German Research Council, the German Centre for Cardiovascular Research, the British Heart Foundation, the European Research Council and Medical Research Scotland.