T cell-selective deletion of Oct1 protects animals from autoimmune neuroinflammation while maintaining neurotropic pathogen response (2019) Tantin

From the article
MS is caused by an abnormal immune response, with a group of T-cells — called CD4- and CD8-positive T-cells — infiltrating the central nervous system and attacking myelin, the protective coat of nerve fibers.

University of Utah School of Medicinehypothesized that the loss of Oct1 could protect against autoimmunity diseases, such as MS, without jeopardizing the capacity of the immune system to fight pathogens or infections.

To test this, they deleted the gene coding for Oct1 specifically in CD4+ T-cells in the experimental autoimmune encephalomyelitis (EAE) mouse model, a well-established model for human MS.

Results showed that mice lacking Oct1 in these T-cells had a lower number of T-cell infiltrates, with theCD4+ T-cells secreting significantly fewer pro-inflammatory cytokines, like interleukin (IL)-17 and interferon-gamma, in the animal’s spinal cords compared to a control and untreated group of mice. Lack of Oct1 also lowered inflammation and eased paralysis.
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Direct link to paper
Open access, https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-019-1523-3
 
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