Ana Almonte-Loya
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Ana Almonte-Loya has a total of 23 co-authors. Here are the top co-authors by number of shared publications:
- Angela M. Detweiler
Genomics and Computational Biology Platforms, Chan Zuckerberg Biohub San Francisco, San Francisco, CA, USA
1 shared publication - Charles R. Langelier
Chan Zuckerberg Biohub, San Francisco, USA
1 shared publication Christina Love
Division of Infectious Diseases, University of California, San Francisco, San Francisco, CA 94143, USA
1 shared publication- Chun Jimmie Ye
Division of Rheumatology, Department of Medicine, University of California, San Francisco, San Francisco, CA, USA
1 shared publication - Cristina M. Lanata
National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA
1 shared publication - Emily C. Lydon
Department of Medicine, Division of Infectious Diseases, University of California, San Francisco
1 shared publication
Latest Publications
- 25 June 2025
- Published by American Association for the Advancement of Science (AAAS) in Science Translational Medicine
- Vol. 17 (804) , eadt5550
Epigenetic attenuation of interferon signaling is associated with aging-related improvements in systemic lupus erythematosus
In the general population, aging is associated with an increase in systemic inflammation and chronic disease burden. However, in systemic lupus erythematosus (SLE), older age is uniquely associated with a decrease in disease activity, suggesting a distinct relationship between aging and inflammation. Using a multiomic approach, we compared aging-related changes in the peripheral blood immune profiles of 287 patients with SLE and 928 healthy controls. In patients with SLE, aging correlated with lower expression of interferon (IFN)–stimulated genes (ISGs) across multiple cell types, decreased plasma IFN-α2, and differential genome methylation. Both patients with SLE and controls demonstrated age-related declines in naïve T cells, but only patients with SLE exhibited increases in CD56 dim natural killer cells with older age. Of the genes both down-regulated and hypermethylated with older age, ISGs were disproportionately represented, suggesting a role for epigenetic silencing. Altogether, we found that patients with SLE exhibit unique aging-related decreases in IFN signaling that correlate with improved disease activity.
- 25 June 2025
- Published by American Association for the Advancement of Science (AAAS) in Science Translational Medicine
- Vol. 17 (804) , eadt5550
Epigenetic attenuation of interferon signaling is associated with aging-related improvements in systemic lupus erythematosus
In the general population, aging is associated with an increase in systemic inflammation and chronic disease burden. However, in systemic lupus erythematosus (SLE), older age is uniquely associated with a decrease in disease activity, suggesting a distinct relationship between aging and inflammation. Using a multiomic approach, we compared aging-related changes in the peripheral blood immune profiles of 287 patients with SLE and 928 healthy controls. In patients with SLE, aging correlated with lower expression of interferon (IFN)–stimulated genes (ISGs) across multiple cell types, decreased plasma IFN-α2, and differential genome methylation. Both patients with SLE and controls demonstrated age-related declines in naïve T cells, but only patients with SLE exhibited increases in CD56 dim natural killer cells with older age. Of the genes both down-regulated and hypermethylated with older age, ISGs were disproportionately represented, suggesting a role for epigenetic silencing. Altogether, we found that patients with SLE exhibit unique aging-related decreases in IFN signaling that correlate with improved disease activity.