Alox15 restrains glycolysis to support M2 macrophage effector function during helminth immunity.

Alox15 is essential for M2 macrophages to trap and kill helminths by restraining glycolysis, despite normal M2 marker expression, revealing a metabolic control mechanism.

• Why it matters: Understanding how macrophages effectively combat helminths is crucial for improving anti-parasitic therapies and tissue repair strategies, yet the metabolic regulation underlying their effector functions remains unclear.
• What they did: The study examined Alox15’s role in macrophage polarization during helminth infection, using functional assays and molecular analysis to compare responses in the presence and absence of Alox15.
• The result: Loss of Alox15 impairs helminth killing due to uncontrolled glycolysis, but lipid-mediated activation of PPAR-delta can restore metabolic balance, enabling effective macrophage effector functions.