Gender Differences In MS Development Explored

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The findings may help the development of improved therapies for both men and women with MS and other autoimmune diseases, study authors concluded.
The findings may help the development of improved therapies for both men and women with MS and other autoimmune diseases, study authors concluded.

The innate lymphoid cell has demonstrated different immune activities in males and females, researchers from the Northwestern Medicine lab note in a study published in The Journal of Immunology.

Typically when female mice are induced with multiple sclerosis (MS), almost all of them get very sick. However, male mice either experience little or no disease. 

In the original study, a group of normal female mice was compared to another group with a genetic mutation in a growth factor receptor (c-kit) that prevents the development of certain immune cells. An accidental switch of female mice with male mice shed light on why women were more likely to develop autoimmune diseases like multiple sclerosis (MS) than men. 

The results showed that the male mice with the mutation got very sick; the results were replicated when the experiment was repeated. Scientists concluded that the mutation was acting differently in males vs. females.

Mice with the c-kit mutation lacked type 2 innate lymphoid cells that are commonly present in bone marrow, lymph nodes, and the thymus. In males, the researchers believe these cells produce a protein to help protect the from the disease by interrupting the damaging immune response. Female mice possess the same cells but they stay inactive and does not exert a protective function.

This was the first study to show that these cells exhibit sex differences in their function and protect in autoimmune disease.

The findings may help the development of improved therapies for both men and women with MS and other autoimmune diseases, study authors concluded. 

More trials are underway to discover potential activators of these cells.

Reference

1. Russi AE, et al. J Immunol. 2015; doi: 10.4049/​jimmunol.1500068 

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