There is a growing need to identify biomarkers of Type 1 diabetes (T1D) progression to determine the efficacy and durability of therapies in clinical trials. Studies have found that a stronger proinflammatory immune landscape predicted faster beta cell decline during partial remission in subjects with T1D. Due to the well-documented, disease-causing role of islet-specific T cells, we aimed to characterise these cells in relation to clinical outcome in subjects with T1D. Using multiplexed HLADR4/DQ8-restricted proinsulin (PI) and PI- hybrid insulin peptide (HIP) tetramers in a comprehensive T cell phenotyping spectral flow cytometry panel, we stained frozen PBMC samples from patients, ex vivo. We found a disease-specific enrichment of CXCR3+ CCR4+ and exhausted regulatory T cell (Treg) phenotypes within islet-specific T cells. Interestingly, these phenotypes which were significantly correlated with shorter partial remission duration in children with T1D. This suggests that the upregulation of specific chemokine receptors on islet-specific T cells may induce their migration to inflamed islets to exacerbate chronic inflammation. This association of CXCR3+ CXCR4+ islet-specific T cells with decreased length of partial remission was also reflected in the global CD4+ and CD8+ T cell compartments, highlighting the potential of these circulating double-positive T cells as robust biomarkers of disease progression and response to therapy in clinical trials.