PLNs may serve as a reservoir for stem-like CD8⁺ T cells that sustain autoimmune responses in T1D. Building on the findings of Peters et al. (5) and previous observations in NOD mice, the model presented here proposes that limited β cell antigen availability in PLNs, combined with the intrinsically low affinity of autoreactive TCRs for β cell antigens, results in weak TCR signaling that favors partial differentiation and maintenance of stem-like properties. This state may be further supported by IL-15 signaling. Stem-like PLN CD8⁺ T cells (red) are characterized by the expression of CXCR3 and self-renewal–associated markers such as BCL2, BCL3, and BCL6, together with TCF1 and TOX. Whether circulating naive-like, islet-reactive CD8⁺ T cells (pink) represent a recirculating counterpart of this PLN cell population remains unknown. Upon migration to pancreatic islets, exposure to higher antigen loads and stronger TCR stimulation may promote further differentiation, acquisition of cytotoxic functions, and eventual exhaustion (brown cells). However, the developmental relationship between PLN stem-like cells and pancreatic effector/exhausted cells remains unresolved, as current evidence demonstrates phenotypic continuity but limited clonal overlap between the two compartments. The figure highlights key hypotheses and outstanding questions emerging from the study by Peters et al., including the roles of recirculation, clonal continuity, and the mechanisms governing the balance between stemness, effector differentiation, and exhaustion.