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More than 1,000 genetic switches reveal why female immunity is different

More than 1,000 genetic switches behave differently in male and female immune cells, helping explain why women are much more vulnerable to autoimmune diseases such as lupus. Female immune systems appear genetically tuned for stronger inflammatory responses—a powerful defense against infection that may also make dangerous immune misfires more likely.

A recent study conducted by the Garvan Institute of Medical Research and UNSW Sydney has uncovered more than 1,000 genetic switches that behave differently in female and male immune cells. This discovery could explain why women are diagnosed with autoimmune diseases more frequently than men. Autoimmune diseases occur when the immune system mistakenly attacks healthy body tissues, with lupus affecting nine women for every one man.

Researchers sequenced over 1.25 million immune cells from nearly 1,000 healthy individuals, revealing that females have greater numbers of B cells and regulatory T cells, and their immune cells show more genetic activity linked to inflammation. These differences may offer protection against viral infections but also increase the risk of autoimmune diseases due to heightened inflammation.

The genetic switches were found primarily on autosomes, the non-sex chromosomes shared by both sexes, rather than the sex chromosomes. This finding challenges the assumption that male-female differences in immune systems are mainly driven by the X and Y chromosomes. The study's lead author, Dr. Seyhan Yazar, emphasizes that the immune system must be studied with sex in mind, as overlooking these differences can limit understanding of diseases and bias treatment options.

Dr. Sara Ballouz, co-senior author, notes that the genetic differences could explain why lupus occurs nine times more often in women than men, although hormones and other factors also play a role. The researchers hope their findings will lead to more personalized autoimmune treatments, with therapies tailored to a patient's specific form of disease rather than a one-size-fits-all approach.

Written by urgent.news from ScienceDaily Health's reporting — not their text. Machine-written — may contain errors; check the original before relying on it.

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