New research reveals that the enzyme ELOVL2, essential in lipid metabolism, plays a pivotal role in maintaining immune system vitality, with its decline accelerating immune aging and potentially increasing cancer risk.
Key Points at a Glance
- ELOVL2 is crucial for synthesizing DHA, a key component of cell membranes.
- Reduced ELOVL2 activity leads to accelerated aging of white blood cells.
- Loss of ELOVL2 alters gene expression linked to blood cancers.
- Findings suggest lipid metabolism is integral to immune system health.
Aging is often associated with a gradual decline in immune function, leading to increased susceptibility to infections and diseases. Recent findings from researchers at UC San Diego and UC Irvine have shed light on a molecular player in this process: the enzyme ELOVL2. Known for its role in lipid metabolism, ELOVL2 is now recognized as a key factor in maintaining the youthful vigor of the immune system.
ELOVL2, short for “elongation of very long chain fatty acids-like 2,” is instrumental in the biosynthesis of docosahexaenoic acid (DHA), an omega-3 fatty acid integral to the structural integrity of cell membranes. DHA’s presence ensures that cell membranes remain flexible and resilient, properties essential for the proper function of immune cells.
The study focused on the bone marrow of mice genetically engineered to lack the Elovl2 gene. The absence of ELOVL2 led to noticeable changes: white blood cells aged more rapidly, and there was a significant alteration in the expression of genes associated with the onset of blood cancers. These findings suggest that ELOVL2’s role extends beyond lipid synthesis; it is a guardian of genomic stability in immune cells.
Dr. Dorota Skowronska-Krawczyk, co-corresponding author of the study, emphasized the importance of DHA in maintaining the flexibility of cell membranes in B cell precursors. “We believe that DHA keeps the cell membranes in the stem cell precursors of B cells flexible and resilient,” she noted. This flexibility is crucial for the proper development and function of B cells, which are central to the adaptive immune response.
The decline of ELOVL2 with age disrupts this balance, leading to stiffer cell membranes and compromised immune cell function. This deterioration not only accelerates the aging of the immune system but also creates an environment conducive to the development of malignancies.
These insights open new avenues for therapeutic interventions aimed at bolstering immune function in the elderly. By targeting the pathways involved in lipid metabolism, particularly those governed by ELOVL2, it may be possible to develop strategies to maintain immune competence and reduce cancer risk in aging populations.
The study underscores the intricate interplay between lipid metabolism and immune system health, highlighting the potential of metabolic enzymes like ELOVL2 as targets for promoting healthy aging.
Source: UC San Diego Today
