Deep immune phenotyping reveals similarities between aging, Down syndrome, and autoimmunity

Abstract

Permutational analysis of the immune system reveals advanced immune aging in individuals with Down syndrome and in individuals with type 1 diabetes.

Investigating sex differences in T regulatory cells from cisgender and transgender healthy individuals and patients with autoimmune inflammatory disease: a cross-sectional study

“…In future studies, it would be useful to investigate additional surface markers for Treg cells and Tresp cells to assess function and partition T cells into sublineages. A wider array of markers were used to this effect by Lambert and colleagues, 32 who revealed important features that vary with autoimmune disease states and by age. Finally, the patients with juvenile-onset SLE were clinically heterogeneous and were on different treatments, presenting possible confounding effects on the immune system, especially considering that dsDNA has previously been shown to correlate negatively with Treg cells in adults with SLE 33 and that immunosuppressive drugs, such as glucocorticoids, hydroxychloroquine, and methotrexate, could influence Treg-cell frequency and function.…”

FRTX-02, a selective and potent inhibitor of DYRK1A, modulates inflammatory pathways in mouse models of psoriasis and atopic dermatitis

“…Inflammatory homeostasis is critically regulated by balanced differentiation of naïve CD4 + T cells into pro-inflammatory T helper (Th) subsets, such as Th17 and Th1, versus anti-inflammatory T regulatory cells (Tregs). The notion that this pathway is dysregulated in people with DS is supported by observations of an increased proportion of Th1, Th17, and Th17/1 cells [ 14 , 15 ] in people with DS. Other Th axis defects associated with DS include impaired Treg function [ 16 ] and impaired response to Tregs [ 14 ].…”

Is any point to be skeptical regarding individuals with Down syndrome who are admitted with COVID-19?

“…As a result, they are more susceptible to infections, particularly bacterial and virus-related pneumonia (12). T cell lineages in adults with Down syndrome have been demonstrated in previous research to display significant evidence of heightened activity even in the absence of any evident infections, a trait presumed to be driven by persistent IFN hyperactivity (13). As a result, patients with Down syndrome have a strong IFN response, which is vital for elevating antiviral responses and triggering and magnifying the cytokine storm (3,14).…”