Paper for discussion: Linking Skin and Joint Inflammation in Psoriatic Arthritis through Shared CD8+ T Cell Clones
Date & Time: March 17, 2026 from 11:00 AM – 12:00 PM Central Time.
Platform: Zoom (Link will be sent via the email address you registered with).
Presented by: Lucy Durham, MBBS, PhD & Leonie Taams, PhD
In this paper, Durham and colleagues report that skin and joint inflammation in psoriatic arthritis
can be linked by CD8+ T cells that exhibit both shared and distinct cellular features across these tissues. Using single‑cell RNA‑seq, TCR repertoire analysis, and spatial transcriptomics, they examined paired skin, synovial tissue, synovial fluid, and peripheral blood samples from the same individuals. Their data reveal an enrichment of type 17 CD8+ tissue-resident memory T (Trm) cells in both the skin and joint, with a stronger interleukin-17 signature in the skin than the joint. Shared CD8⁺ T‑cell clones across the two tissues further support coordinated immune activation. At the same time, transcriptomic differences among CD8⁺ T‑cell subsets — including Trm cells — between skin and joint sites suggest that psoriatic arthritis and psoriasis involve overlapping yet distinct CD8⁺ T‑cell–driven mechanisms.
Paper for discussion: CAR Treg cells mediate linked suppression and infectious tolerance in islet transplantation in mice
Date & Time: January 28, 2026 from 10:00 AM – 11:00 AM Central Time.
Platform: Zoom (Link will be sent via the email address you registered with).
Using a mouse model of HLA-A2+ islet transplantation followed by diabetogenic T cell transfer, we showed that HLA-A2-specific chimeric antigen receptor regulatory T cells (A2-CAR Tregs) protected the HLA-A2+ islet graft against autoimmune attack, as was hypothesized based on previous reports demonstrating that engineered Tregs effectively protect tissues expressing their cognate antigen. In addition, we found that A2-CAR Treg treatment mediated linked suppression by also protecting the endogenous pancreas that lacked the expression of HLA-A2. Further, this protection persisted beyond the removal of A2-CAR Tregs, demonstrating infectious tolerance and the immune system’s reprograming for tolerance. This study suggests that engineered Tregs may be able to establish long-lived tolerance of cognate and distinct antigens with a single, transient dose.
Presented by: Christine Wardell, PhD Student & Megan Levings, PhD