| First Author | Cordeiro B | Year | 2024 |
| Journal | Cell Metab | PubMed ID | 39168127 |
| Mgi Jnum | J:353957 | Mgi Id | MGI:7717278 |
| Doi | 10.1016/j.cmet.2024.07.017 | Citation | Cordeiro B, et al. (2024) Obesity intensifies sex-specific interferon signaling to selectively worsen central nervous system autoimmunity in females. Cell Metab |
| abstractText | Obesity has been implicated in the rise of autoimmunity in women. We report that obesity induces a serum protein signature that is associated with T helper 1 (Th1), interleukin (IL)-17, and multiple sclerosis (MS) signaling pathways selectively in human females. Females, but not male mice, subjected to diet-induced overweightness/obesity (DIO) exhibited upregulated Th1/IL-17 inflammation in the central nervous system during experimental autoimmune encephalomyelitis, a model of MS. This was associated with worsened disability and a heightened expansion of myelin-specific Th1 cells in the peripheral lymphoid organs. Moreover, at steady state, DIO increased serum levels of interferon (IFN)-alpha and potentiated STAT1 expression and IFN-gamma production by naive CD4(+) T cells uniquely in female mice. This T cell phenotype was driven by increased adiposity and was prevented by the removal of ovaries or knockdown of the type I IFN receptor in T cells. Our findings offer a mechanistic explanation of how obesity enhances autoimmunity. |
